Journal Description
Current Issues in Molecular Biology
Current Issues in Molecular Biology
is an international, scientific, peer-reviewed, open access journal on molecular biology, published monthly online by MDPI (from Volume 43 Issue 1-2021).
- Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
- High Visibility: indexed within Scopus, SCIE (Web of Science), PMC, PubMed, Embase, CAPlus / SciFinder, FSTA, AGRIS, and other databases.
- Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 16.8 days after submission; acceptance to publication is undertaken in 2.7 days (median values for papers published in this journal in the first half of 2024).
- Recognition of Reviewers: APC discount vouchers, optional signed peer review, and reviewer names are published annually in the journal.
Impact Factor:
2.8 (2023);
5-Year Impact Factor:
2.9 (2023)
Latest Articles
Functional Activities and Mechanisms of Aronia melanocarpa in Our Health
Curr. Issues Mol. Biol. 2024, 46(8), 8071-8087; https://doi.org/10.3390/cimb46080477 - 26 Jul 2024
Abstract
Aronia melanocarpa, known as black chokeberry, is rich in polyphenols, comprising flavonoids, such as anthocyanins, flavanols, and flavonols, and phenolic acids, such as chlorogenic acid. These polyphenols endow Aronia melanocarpa with preventive and therapeutic properties against various human diseases. Aronia melanocarpa has
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Aronia melanocarpa, known as black chokeberry, is rich in polyphenols, comprising flavonoids, such as anthocyanins, flavanols, and flavonols, and phenolic acids, such as chlorogenic acid. These polyphenols endow Aronia melanocarpa with preventive and therapeutic properties against various human diseases. Aronia melanocarpa has beneficial effects against diseases such as diabetes, inflammation, and hypertension. Considering the diverse functional components of Aronia melanocarpa, its efficacy in disease prevention and treatment can operate through multiple pathways, offering a more robust approach to disease control. This review covers the latest research results on the functional components of Aronia melanocarpa and their effects on human diseases.
Full article
(This article belongs to the Special Issue Molecular Insights into Food-Derived Natural Products and Their Biological Activities)
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Open AccessReview
Advances in Microflow Cytometry-Based Molecular Detection Methods for Improved Future MDS Cancer Diagnosis
by
Marc Gonsalves, Andres Escobar, Ahmad Diaa Altarabishi and Chang-Qing Xu
Curr. Issues Mol. Biol. 2024, 46(8), 8053-8070; https://doi.org/10.3390/cimb46080476 - 26 Jul 2024
Abstract
Myelodysplastic syndromes (MDS) are a rare form of early-stage blood cancer that typically leads to leukemia and other deadly complications. The typical diagnosis for MDS involves a mixture of blood tests, a bone marrow biopsy, and genetic analysis. Flow cytometry has commonly been
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Myelodysplastic syndromes (MDS) are a rare form of early-stage blood cancer that typically leads to leukemia and other deadly complications. The typical diagnosis for MDS involves a mixture of blood tests, a bone marrow biopsy, and genetic analysis. Flow cytometry has commonly been used to analyze these types of samples, yet there still seems to be room for advancement in several areas, such as the limit of detection, turnaround time, and cost. This paper explores recent advancements in microflow cytometry technology and how it may be used to supplement conventional methods of diagnosing blood cancers, such as MDS and leukemia, through flow cytometry. Microflow cytometry, a more recent adaptation of the well-researched and conventional flow cytometry techniques, integrated with microfluidics, demonstrates significant potential in addressing many of the shortcomings flow cytometry faces when diagnosing a blood-related disease such as MDS. The benefits that this platform brings, such as portability, processing speed, and operating cost, exemplify the importance of exploring microflow cytometry as a point-of-care (POC) diagnostic device for MDS and other forms of blood cancer.
Full article
(This article belongs to the Special Issue The Contribution and Application of Molecular Biology in the Applied Biosciences — Focusing on Medicine, Biomaterials and Tissue Engineering Fields)
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Open AccessReview
Neuraminidase-1 (NEU1): Biological Roles and Therapeutic Relevance in Human Disease
by
Jingxia Du, Hanqi Shui, Rongjun Chen, Yibo Dong, Chengyao Xiao, Yue Hu and Nai-Kei Wong
Curr. Issues Mol. Biol. 2024, 46(8), 8031-8052; https://doi.org/10.3390/cimb46080475 - 26 Jul 2024
Abstract
Neuraminidases catalyze the desialylation of cell-surface glycoconjugates and play crucial roles in the development and function of tissues and organs. In both physiological and pathophysiological contexts, neuraminidases mediate diverse biological activities via the catalytic hydrolysis of terminal neuraminic, or sialic acid residues in
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Neuraminidases catalyze the desialylation of cell-surface glycoconjugates and play crucial roles in the development and function of tissues and organs. In both physiological and pathophysiological contexts, neuraminidases mediate diverse biological activities via the catalytic hydrolysis of terminal neuraminic, or sialic acid residues in glycolipid and glycoprotein substrates. The selective modulation of neuraminidase activity constitutes a promising strategy for treating a broad spectrum of human pathologies, including sialidosis and galactosialidosis, neurodegenerative disorders, cancer, cardiovascular diseases, diabetes, and pulmonary disorders. Structurally distinct as a large family of mammalian proteins, neuraminidases (NEU1 through NEU4) possess dissimilar yet overlapping profiles of tissue expression, cellular/subcellular localization, and substrate specificity. NEU1 is well characterized for its lysosomal catabolic functions, with ubiquitous and abundant expression across such tissues as the kidney, pancreas, skeletal muscle, liver, lungs, placenta, and brain. NEU1 also exhibits a broad substrate range on the cell surface, where it plays hitherto underappreciated roles in modulating the structure and function of cellular receptors, providing a basis for it to be a potential drug target in various human diseases. This review seeks to summarize the recent progress in the research on NEU1-associated diseases and highlight the mechanistic implications of NEU1 in disease pathogenesis. An improved understanding of NEU1-associated diseases should help accelerate translational initiatives to develop novel or better therapeutics.
Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Open AccessArticle
Genome-Wide Identification and Expression Analysis of the Sweet Cherry Whirly Gene Family
by
Lili Wang, Qiandong Hou and Guang Qiao
Curr. Issues Mol. Biol. 2024, 46(8), 8015-8030; https://doi.org/10.3390/cimb46080474 - 26 Jul 2024
Abstract
Sweet cherry (Prunus avium) is one of the economically valuable horticultural fruit trees and it is widely cultivated throughout the world. Whirly (WHY) genes are a unique gene family with few members and have important biological functions in plant growth, development,
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Sweet cherry (Prunus avium) is one of the economically valuable horticultural fruit trees and it is widely cultivated throughout the world. Whirly (WHY) genes are a unique gene family with few members and have important biological functions in plant growth, development, and response to abiotic stress. This study utilized whole-genome identification to conduct a comprehensive analysis of the WHY genes in sweet cherry and examined their transcription levels in different tissues and under abiotic stress to explore their functions. Two WHY genes were identified in the sweet cherry genome and named PavWHY1 and PavWHY2, respectively, based on their homology with those in Arabidopsis thaliana. Both genes have theoretical isoelectric points greater than seven and are hydrophilic proteins, suggesting that they may be localized in plastids. The two genes are evolutionarily classified into two categories, with large differences in gene structure, and highly similar protein tertiary structures, and both have conserved domains of WHY. PavWHY1 and PavWHY2 are collinear with AtWHY1 and AtWHY2, respectively. The promoter sequence contains cis-acting elements related to hormones and abiotic stress, which are differentially expressed during flower bud differentiation, fruit development, and cold accumulation. qRT–PCR showed that PavWHY1 and PavWHY2 were differentially expressed in flower and fruit development and responded to low temperature and exogenous ABA treatment. The recombinant plasmid pGreenII-0800-Luc with the promoters of these two genes can activate luciferase expression in tobacco. Protein interaction predictions indicate that these gene products may interact with other proteins. This study reveals the molecular features, evolutionary relationships, and expression patterns of sweet cherry WHY genes, and investigates the activities of their promoters, which lays the foundation for further exploration of their biological functions and provides new insights into the WHY gene family in Rosaceae.
Full article
(This article belongs to the Special Issue Functional Genomics and Comparative Genomics Analysis in Plants, 2nd Edition)
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Open AccessArticle
Transcriptome Analyses of Liver Sinusoidal Endothelial Cells Reveal a Consistent List of Candidate Genes Associated with Endothelial Dysfunction and the Fibrosis Progression
by
Penghui Li, Wenjie Xie, Hongjin Wei, Fan Yang, Yan Chen and Yinxiong Li
Curr. Issues Mol. Biol. 2024, 46(8), 7997-8014; https://doi.org/10.3390/cimb46080473 - 25 Jul 2024
Abstract
Liver fibrosis is an important step in the transformation of chronic liver disease into cirrhosis and liver cancer, and structural changes and functional disorders of liver sinusoidal endothelial cells (LSECs) are early events in the occurrence of liver fibrosis. Therefore, it is necessary
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Liver fibrosis is an important step in the transformation of chronic liver disease into cirrhosis and liver cancer, and structural changes and functional disorders of liver sinusoidal endothelial cells (LSECs) are early events in the occurrence of liver fibrosis. Therefore, it is necessary to identify the key regulatory genes of endothelial dysfunction in the process of liver fibrosis to provide a reference for the diagnosis and treatment of liver fibrosis. In this study, we identified 230 common differentially expressed genes (Co-DEGs) by analyzing transcriptomic data of primary LSECs from three different liver fibrosis mouse models (carbon tetrachloride; choline-deficient, l-amino acid-defined diet; and nonalcoholic steatohepatitis). Enrichment analysis revealed that the Co-DEGs were mainly involved in regulating the inflammatory response, immune response, angiogenesis, formation and degradation of the extracellular matrix, and mediating chemokine-related pathways. A Venn diagram analysis was used to identify 17 key genes related to the progression of liver cirrhosis. Regression analysis using the Lasso–Cox method identified genes related to prognosis among these key genes: SOX4, LGALS3, SERPINE2, CD52, and LPXN. In mouse models of liver fibrosis (bile duct ligation and carbon tetrachloride), all five key genes were upregulated in fibrotic livers. This study identified key regulatory genes for endothelial dysfunction in liver fibrosis, namely SOX4, LGALS3, SERPINE2, CD52, and LPXN, which will provide new targets for the development of therapeutic strategies targeting endothelial dysfunction in LSECs and liver fibrosis.
Full article
(This article belongs to the Section Molecular Medicine)
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Open AccessArticle
An Experimental Murine Model to Study Lipoatrophia Semicircularis
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María Angustias Palomar-Gallego, Julio Ramiro-Bargueño, Esther Cuerda-Galindo, Rafael Linares-García-Valdecasas, Stella M. Gómez-Sánchez, José Delcan and Gema Díaz-Gil
Curr. Issues Mol. Biol. 2024, 46(8), 7986-7996; https://doi.org/10.3390/cimb46080472 - 25 Jul 2024
Abstract
Lipoatrophia semicircularis is a benign pathology characterized by subcutaneous tissue atrophy that affects the skin and related structures. Its etiology remains unclear; however, in the recent few years, it has been proposed that electrostatic charges could be a potential factor. Based on this
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Lipoatrophia semicircularis is a benign pathology characterized by subcutaneous tissue atrophy that affects the skin and related structures. Its etiology remains unclear; however, in the recent few years, it has been proposed that electrostatic charges could be a potential factor. Based on this hypothesis, the aim of this work is to study the cause–effect relation between electrostatic energy and LS, providing insights into the molecular mechanisms. For this purpose, an experimental murine model was created using obese mice. One group served as a control and the other groups involved charging clothes with varying connections to the ground: through the skin, through the clothes or not connected to the ground). Skin biopsies showed that the most significant lesions, including lipophagic granulomas with inflammatory infiltrate, were found in the first group (connected to the ground through the skin). Lipophagic reactions without an inflammatory infiltrate were observed in the other groups subjected to electrical discharges. In the control mice, no histological changes were observed. Oxidative processes were also measured in lower limbs tissue. Malondialdehyde levels significantly increased in the lower limbs after electrostatic discharges. However, the presence of ground through a wire attached to highly conductive clothes around the thigh significantly reduced the effect of electrostatic charges on lipid peroxidation. To our knowledge, this is the first study in which an experimental model has been used to reproduce LS induced by electrostatic energy, suggesting a cause–effect relationship between electrostatic charge and discharge with fat tissue lesion.
Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Open AccessCase Report
Frequency of Deleterious Germline Variants in HER2-Low Breast Cancer Patients Using a Hereditary Multipanel Gene Testing
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Janaina Pontes Batista Cassoli, Ítalo Fernandes, Leonardo Carvalho, Milena Fernandes, Ana Fernanda Centrone, Letícia Taniwaki, Rita de Cássia Lima, Uelson Donizeti Rocioli Junior, Igor Wanderley Reis Dias, Patrícia Taranto, Juliana Beal, Fernanda Teresa de Lima, Fernando Moura, Miguel Cendoroglo, Sergio Eduardo Alonso Araújo and Pedro Luiz Serrano Uson Junior
Curr. Issues Mol. Biol. 2024, 46(8), 7976-7985; https://doi.org/10.3390/cimb46080471 - 25 Jul 2024
Abstract
HER2-Low is defined as low levels of HER2 expression, based on a score of 1+ on immunohistochemical (IHC) assay or as an IHC score of 2+ and negative results on in situ hybridization (ISH or FISH). They are a heterogeneous population of breast
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HER2-Low is defined as low levels of HER2 expression, based on a score of 1+ on immunohistochemical (IHC) assay or as an IHC score of 2+ and negative results on in situ hybridization (ISH or FISH). They are a heterogeneous population of breast cancers that vary in prognosis and sensitivity to systemic treatments. The frequency and clinical characteristics of pathogenic germline variants (PGVs) in HER2-Low breast cancer (BC) patients is not defined. We analyzed results from patients with BC who underwent multi-gene panel testing (MGPT) (maximum 145 genes) between 2018–2019. We reclassified HER-2 status accordingly. Relationships between the variables of interest were assessed by adopting the proportional regression Cox models. Of a total of 167 BC patients who underwent MGPT, half were hormone-receptor-positive. The median age was 45 years. About two thirds of the patients were in the earlier stage of BC. A total of 57% of the cases were reclassified as HER-2-negative or -Low. PGVs were found in 19% of the patients overall, as follows: seven BRCA1, four BRCA2, two ATM, one ATR, two CFTR, three CHEK2, one FANCA, one MERTK, one MLH1, three MUTYH, one RAD50, three RAD51C, one RECQL4, and two TP53 mutations. In HER2-Low, 26.5% of the patients had PGVs, and in the overall cohort, this was 19.8%. In conclusion, differences in the prevalence of deleterious germline mutations in HER2-Low BC patients compared to non-HER2-Low BC patients were identified. Similar alterations in BRCA were observed in this group of patients compared to the overall cohort. Germline genetic tests should be evaluated in larger cohorts of patients with HER2-Low status to better address the findings.
Full article
(This article belongs to the Special Issue Genomic Analysis of Common Disease)
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Open AccessReview
Aquaporin Modulation by Cations, a Review
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Robin Mom, Vincent Mocquet, Daniel Auguin and Stéphane Réty
Curr. Issues Mol. Biol. 2024, 46(8), 7955-7975; https://doi.org/10.3390/cimb46080470 - 24 Jul 2024
Abstract
Aquaporins (AQPs) are transmembrane channels initially discovered for their role in water flux facilitation through biological membranes. Over the years, a much more complex and subtle picture of these channels appeared, highlighting many other solutes accommodated by AQPs and a dense regulatory network
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Aquaporins (AQPs) are transmembrane channels initially discovered for their role in water flux facilitation through biological membranes. Over the years, a much more complex and subtle picture of these channels appeared, highlighting many other solutes accommodated by AQPs and a dense regulatory network finely tuning cell membranes’ water permeability. At the intersection between several transduction pathways (e.g., cell volume regulation, calcium signaling, potassium cycling, etc.), this wide and ancient protein family is considered an important therapeutic target for cancer treatment and many other pathophysiologies. However, a precise and isoform-specific modulation of these channels function is still challenging. Among the modulators of AQPs functions, cations have been shown to play a significant contribution, starting with mercury being historically associated with the inhibition of AQPs since their discovery. While the comprehension of AQPs modulation by cations has improved, a unifying molecular mechanism integrating all current knowledge is still lacking. In an effort to extract general trends, we reviewed all known modulations of AQPs by cations to capture a first glimpse of this regulatory network. We paid particular attention to the associated molecular mechanisms and pinpointed the residues involved in cation binding and in conformational changes tied up to the modulation of the channel function.
Full article
(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2024)
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Open AccessArticle
ALA Promotes Sucrose Accumulation in Early Peach Fruit by Regulating SPS Activity
by
Zheng Chen, Xin Guo, Jinhua Du and Mingliang Yu
Curr. Issues Mol. Biol. 2024, 46(8), 7944-7954; https://doi.org/10.3390/cimb46080469 - 24 Jul 2024
Abstract
5-Aminolevulinic acid (ALA), as a novel plant growth regulator, is a critical precursor for the biosynthesis of porphyrin compounds in all organisms. Many studies have reported that exogenous ALA treatment could improve fruit sweetness. However, the mechanism by which ALA promotes the increase
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5-Aminolevulinic acid (ALA), as a novel plant growth regulator, is a critical precursor for the biosynthesis of porphyrin compounds in all organisms. Many studies have reported that exogenous ALA treatment could improve fruit sweetness. However, the mechanism by which ALA promotes the increase in sugar content in fruit remains unclear. In this study, we found that ALA significantly promoted sucrose accumulation and SPS (sucrose phosphate synthase) activity in peach fruit. At 14, 28, 42, 50 and 60 days after ALA treatment, sucrose content of fruit was increased by 23%, 43%, 37%, 40% and 16%, respectively, compared with control treatment, and SPS enzyme activity was increased by 21%, 28%, 47%, 37% and 29%, respectively. Correlation analysis showed that the sucrose content of peach fruit under ALA treatment was significantly positively correlated with SPS activity. Subsequently, bioinformatics was used to identify SPS gene family members in peach fruit, and it was found that there were four members of the PpSPS gene family, distributed on chromosomes 1, 7 and 8, named PpSPS1, PpSPS2, PpSPS3 and PpSPS4, respectively. The results of qRT-PCR showed that PpSPS2 and PpSPS3 were highly expressed in response to ALA during fruit development, and the expression of PpSPS2 was positively correlated with SPS activity and sucrose accumulation in peach fruit. The results of tobacco subcellular localization showed that PpSPS2 was mainly distributed in the cytoplasm and nucleus, while PpSPS3 was mainly distributed in the nucleus. The results of this study will lay the foundation for further study on the functions of PpSPS and the regulation of sugar metabolism during the development and ripening of peach fruit by ALA.
Full article
(This article belongs to the Section Molecular Plant Sciences)
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Open AccessReview
Capsaicin: Emerging Pharmacological and Therapeutic Insights
by
Elena Madalina Petran, Argyrios Periferakis, Lamprini Troumpata, Aristodemos-Theodoros Periferakis, Andreea-Elena Scheau, Ioana Anca Badarau, Konstantinos Periferakis, Ana Caruntu, Ilinca Savulescu-Fiedler, Romina-Marina Sima, Daniela Calina, Carolina Constantin, Monica Neagu, Constantin Caruntu and Cristian Scheau
Curr. Issues Mol. Biol. 2024, 46(8), 7895-7943; https://doi.org/10.3390/cimb46080468 - 24 Jul 2024
Abstract
Capsaicin, the most prominent pungent compound of chilli peppers, has been used in traditional medicine systems for centuries; it already has a number of established clinical and industrial applications. Capsaicin is known to act through the TRPV1 receptor, which exists in various tissues;
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Capsaicin, the most prominent pungent compound of chilli peppers, has been used in traditional medicine systems for centuries; it already has a number of established clinical and industrial applications. Capsaicin is known to act through the TRPV1 receptor, which exists in various tissues; capsaicin is hepatically metabolised, having a half-life correlated with the method of application. Research on various applications of capsaicin in different formulations is still ongoing. Thus, local capsaicin applications have a pronounced anti-inflammatory effect, while systemic applications have a multitude of different effects because their increased lipophilic character ensures their augmented bioavailability. Furthermore, various teams have documented capsaicin’s anti-cancer effects, proven both in vivo and in vitro designs. A notable constraint in the therapeutic effects of capsaicin is its increased toxicity, especially in sensitive tissues. Regarding the traditional applications of capsaicin, apart from all the effects recorded as medicinal effects, the application of capsaicin in acupuncture points has been demonstrated to be effective and the combination of acupuncture and capsaicin warrants further research. Finally, capsaicin has demonstrated antimicrobial effects, which can supplement its anti-inflammatory and anti-carcinogenic actions.
Full article
(This article belongs to the Special Issue Latest Review Papers in Molecular Biology 2024)
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Open AccessArticle
Injection of Adipose-Derived Mesenchymal Stem/Stromal Cells Suppresses Muscle Atrophy Markers and Adipogenic Markers in a Rat Fatty Muscle Degeneration Model
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Sai Koung Ngeun, Miki Shimizu and Masahiro Kaneda
Curr. Issues Mol. Biol. 2024, 46(8), 7877-7894; https://doi.org/10.3390/cimb46080467 - 24 Jul 2024
Abstract
Fatty muscle degeneration and muscle atrophy have not been successfully treated due to their irreversible pathology. This study evaluated the efficacy of rat adipose-derived mesenchymal stem/stromal cells (ADP MSCs) in treating fatty muscle degeneration (FD). A total of 36 rats were divided into
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Fatty muscle degeneration and muscle atrophy have not been successfully treated due to their irreversible pathology. This study evaluated the efficacy of rat adipose-derived mesenchymal stem/stromal cells (ADP MSCs) in treating fatty muscle degeneration (FD). A total of 36 rats were divided into three groups: the control (C) group (n = 12); FD model group, generated by sciatic nerve crushing (n = 12); and the group receiving ADP MSC treatment for FD (FD+MSCs) (n = 12). In Group FD+MSCs, ADP MSCs were injected locally into the gastrocnemius muscle one week after the FD model was created (Day 8). On Day 22 (n = 18) and Day 43 (n = 18), muscle morphology, histopathology, and molecular analyses (inflammation, muscle atrophy, adipocytes, and muscle differentiation markers) were performed. In Group FD+MSCs, the formation of immature myofibers was observed on Day 22, and mitigation of fatty degeneration and muscle atrophy progression was evident on Day 43. Gene expression of muscle atrophy markers (FBXO32, TRIM63, and FOXO1) and adipogenic markers (ADIPOQ, PPARG, FABP4, and PDGFRA) was lower in Group FD+MSCs than Group FD on Day 43. ADP MSCs induce anti-inflammatory effects, inhibit fat accumulation, and promote muscle regeneration, highlighting their potential as promising therapy for FD and atrophy.
Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Open AccessArticle
Identifying Universal Fish Biomarker Genes in Response to PCB126 Exposure by Comparative Transcriptomic Analyses
by
Ira Agrawal, Ai Qi Lee and Zhiyuan Gong
Curr. Issues Mol. Biol. 2024, 46(8), 7862-7876; https://doi.org/10.3390/cimb46080466 - 23 Jul 2024
Abstract
Water pollution remains a major environmental concern, with increased toxic by-products being released into water bodies. Many of these chemical contaminants persist in the environment and bio-accumulate in aquatic organisms. At present, toxicological tests are mostly based on laboratory tests, and effective methods
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Water pollution remains a major environmental concern, with increased toxic by-products being released into water bodies. Many of these chemical contaminants persist in the environment and bio-accumulate in aquatic organisms. At present, toxicological tests are mostly based on laboratory tests, and effective methods for monitoring wild aquatic environments remain lacking. In the present study, we used a well-characterized toxic chemical, 3,3′,4,4′,5-polychlorinated biphenyl (PCB126), as an example to try to identify common biomarker genes to be used for predictive toxicity of this toxic substance. First, we used two laboratory fish models, the zebrafish (Danio rerio) and medaka (Oryzias latipes), to expose PCB126 to obtain liver transcriptomic data by RNA-seq. Comparative transcriptomic analyses indicated generally conserved and concerted changes from the two species, thus validating the transcriptomic data for biomarker gene selection. Based on the common up- and downregulated genes in the two species, we selected nine biomarker genes to further test in other fish species. The first validation experiment was carried out using the third fish species, Mozambique tilapia (Oreochromis mossambicus), and essentially, all these biomarker genes were validated for consistent responses with the two laboratory fish models. Finally, to develop universal PCR primers suitable for potentially all teleost fish species, we designed degenerate primers and tested them in the three fish species as well as in another fish species without a genomic sequence available: guppy (Poecilia reticulata). We found all the biomarker genes showed consistent response to PCB126 exposure in at least 50% of the species. Thus, our study provides a promising strategy to identify common biomarker genes to be used for teleost fish analyses. By using degenerate PCR primers and analyzing multiple biomarker genes, it is possible to develop diagnostic PCR arrays to predict water contamination from any wild fish species sampled in different water bodies.
Full article
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Open AccessHypothesis
The Current Landscape of Hypotheses Describing the Contribution of CD4+ Heterogeneous Populations to ALS
by
Mariusz Sacharczuk, Michel-Edwar Mickael, Norwin Kubick, Agnieszka Kamińska, Jarosław Olav Horbańczuk, Atanas G. Atanasov, Piotr Religa and Michał Ławiński
Curr. Issues Mol. Biol. 2024, 46(8), 7846-7861; https://doi.org/10.3390/cimb46080465 - 23 Jul 2024
Abstract
Amyotrophic Lateral Sclerosis (ALS) is a poorly understood and fatal disease. It has a low prevalence and a 2–4 year survival period. Various theories and hypotheses relating to its development process have been proposed, albeit with no breakthrough in its treatment. Recently, the
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Amyotrophic Lateral Sclerosis (ALS) is a poorly understood and fatal disease. It has a low prevalence and a 2–4 year survival period. Various theories and hypotheses relating to its development process have been proposed, albeit with no breakthrough in its treatment. Recently, the role of the adaptive immune system in ALS, particularly CD4+ T cells, has begun to be investigated. CD4+ T cells are a heterogeneous group of immune cells. They include highly pro-inflammatory types such as Th1 and Th17, as well as highly anti-inflammatory cells such as Tregs. However, the landscape of the role of CD4+ T cells in ALS is still not clearly understood. This review covers current hypotheses that elucidate how various CD4+ T cells can contribute to ALS development. These hypotheses include the SWITCH model, which suggests that, in the early stages of the disease, Tregs are highly capable of regulating the immune response. However, in the later stages of the disease, it seems that pro-inflammatory cells such as Th1 and Th17 are capable of overwhelming Treg function. The reason why this occurs is not known. Several research groups have proposed that CD4+ T cells as a whole might experience aging. Others have proposed that gamma delta T cells might directly target Tregs. Additionally, other research groups have argued that less well-known CD4+ T cells, such as Emoes+ CD4+ T cells, may be directly responsible for neuron death by producing granzyme B. We propose that the ALS landscape is highly complicated and that there is more than one feasible hypothesis. However, it is critical to take into consideration the differences in the ability of different populations of CD4+ T cells to infiltrate the blood–brain barrier, taking into account the brain region and the time of infiltration. Shedding more light on these still obscure factors can help to create a personalized therapy capable of regaining the balance of power in the battle between the anti-inflammatory and pro-inflammatory cells in the central nervous system of ALS patients.
Full article
(This article belongs to the Special Issue The Molecular Roles of CD4+ T Cell Subsets in Neuropathological Diseases—Unraveling Diverse Interactions and Therapeutic Potentials)
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Open AccessArticle
Endothelin-3 Suppresses Luteinizing Hormone Receptor Expression by Regulating the cAMP-PKA Pathway in Hen Granulosa Cells
by
Yurong Tai, Deping Han, Xue Yang, Ganxian Cai, Huaiyu Li, Junying Li and Xuemei Deng
Curr. Issues Mol. Biol. 2024, 46(8), 7832-7845; https://doi.org/10.3390/cimb46080464 - 23 Jul 2024
Abstract
Previous research identified the expression of EDN3 in granulosa cells of preovulatory follicles in chickens. Notably, the expression level of EDN3 in Silky Fowl with low egg-laying performance was significantly higher than that in high-yield laying breed White Leghorn. Given the crucial role
[...] Read more.
Previous research identified the expression of EDN3 in granulosa cells of preovulatory follicles in chickens. Notably, the expression level of EDN3 in Silky Fowl with low egg-laying performance was significantly higher than that in high-yield laying breed White Leghorn. Given the crucial role of granulosa cells in follicular development and maturation, it is very important to study the effect of EDN3 on the biological function of granular cells. In this study, an EDN3 overexpression plasmid was constructed and transfected into granular cells. The viability of these cells was detected using quantiative (qPCR), Cell Counting Kit-8 (CCK8), and 5-Ethynyl-2′-deoxyuridine (EdU) assays. Gonadal hormone synthesis was detected using enzyme-linked immunosorbent assay (ELISA) techniques. Finally, transcriptome sequencing was employed to identify differentially expressed genes. Result showed thatoverexpression of EDN3 was observed to promote cell viability. In addition, it significantly inhibits the expressions of LHR and cAMP-PKA signaling pathways. Cell transcriptome sequencing data displayed that EDN3 can upregulate energy metabolism and immune-related signaling pathways, whereas follicle maturation and the GnRH signaling pathway were downregulated. In conclusion, this study demonstrates that EDN3 can enhance granulosa cell viability and inhibit the expression of LHCGR, a process likely mediated through the cAMP-PKA signaling pathway. However, further evidence is required to substantiate the regulatory relationship between EDN3 and the cAMP-PKA signaling pathway.
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(This article belongs to the Collection Application of Natural and Pseudo Natural Products in Drug Discovery and Development)
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Open AccessReview
The Microbiota in Cancer: A Secondary Player or a Protagonist?
by
Ana María Gómez García, Francisco López Muñoz and Eduardo García-Rico
Curr. Issues Mol. Biol. 2024, 46(8), 7812-7831; https://doi.org/10.3390/cimb46080463 - 23 Jul 2024
Abstract
The intestinal microbiota and the human body are in a permanent interaction. There is a symbiotic relationship in which the microbiota plays a vitally important role in the performance of numerous functions, including digestion, metabolism, the development of lymphoid tissue, defensive functions, and
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The intestinal microbiota and the human body are in a permanent interaction. There is a symbiotic relationship in which the microbiota plays a vitally important role in the performance of numerous functions, including digestion, metabolism, the development of lymphoid tissue, defensive functions, and other processes. It is a true metabolic organ essential for life and has potential involvement in various pathological states, including cancer and pathologies other than those of a digestive nature. A growing topic of great interest for its implications is the relationship between the microbiota and cancer. Dysbiosis plays a role in oncogenesis, tumor progression, and even the response to cancer treatment. The effect of the microbiota on tumor development goes beyond a local effect having a systemic effect. Another aspect of great interest regarding the intestinal microbiota is its relationship with drugs, modifying their activity. There is increasing evidence that the microbiota influences the therapeutic activity and side effects of antineoplastic drugs and also modulates the response of several tumors to antineoplastic therapy through immunological circuits. These data suggest the manipulation of the microbiota as a possible adjuvant to improve oncological treatment. Is it possible to manipulate the microbiota for therapeutic purposes?
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(This article belongs to the Special Issue The 25th Anniversary of CIMB: Perspectives in Molecular Biology)
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Open AccessReview
Phagocytosis Checkpoints in Glioblastoma: CD47 and Beyond
by
Amber Afzal, Zobia Afzal, Sophia Bizink, Amanda Davis, Sara Makahleh, Yara Mohamed and Salvatore J. Coniglio
Curr. Issues Mol. Biol. 2024, 46(8), 7795-7811; https://doi.org/10.3390/cimb46080462 - 23 Jul 2024
Abstract
Glioblastoma multiforme (GBM) is one of the deadliest human cancers with very limited treatment options available. The malignant behavior of GBM is manifested in a tumor which is highly invasive, resistant to standard cytotoxic chemotherapy, and strongly immunosuppressive. Immune checkpoint inhibitors have recently
[...] Read more.
Glioblastoma multiforme (GBM) is one of the deadliest human cancers with very limited treatment options available. The malignant behavior of GBM is manifested in a tumor which is highly invasive, resistant to standard cytotoxic chemotherapy, and strongly immunosuppressive. Immune checkpoint inhibitors have recently been introduced in the clinic and have yielded promising results in certain cancers. GBM, however, is largely refractory to these treatments. The immune checkpoint CD47 has recently gained attention as a potential target for intervention as it conveys a “don’t eat me” signal to tumor-associated macrophages (TAMs) via the inhibitory SIRP alpha protein. In preclinical models, the administration of anti-CD47 monoclonal antibodies has shown impressive results with GBM and other tumor models. Several well-characterized oncogenic pathways have recently been shown to regulate CD47 expression in GBM cells and glioma stem cells (GSCs) including Epidermal Growth Factor Receptor (EGFR) beta catenin. Other macrophage pathways involved in regulating phagocytosis including TREM2 and glycan binding proteins are discussed as well. Finally, chimeric antigen receptor macrophages (CAR-Ms) could be leveraged for greatly enhancing the phagocytosis of GBM and repolarization of the microenvironment in general. Here, we comprehensively review the mechanisms that regulate the macrophage phagocytosis of GBM cells.
Full article
(This article belongs to the Special Issue Future Challenges of Targeted Therapy of Cancers: 2nd Edition)
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Open AccessArticle
Astragalus Polysaccharides and Metformin May Have Synergistic Effects on the Apoptosis and Ferroptosis of Lung Adenocarcinoma A549 Cells
by
I-Yun Lee, Ting-Chung Wang, Yu-Jen Kuo, Wei-Tai Shih, Pei-Rung Yang, Cheng-Ming Hsu, Yu-Shih Lin, Ren-Shyang Kuo and Ching-Yuan Wu
Curr. Issues Mol. Biol. 2024, 46(8), 7782-7794; https://doi.org/10.3390/cimb46080461 - 23 Jul 2024
Abstract
Astragalus polysaccharides (APSs), the compounds extracted from the common herb Astragalus membranaceus, have been extensively studied for their antitumor properties. In this study, we investigated the effect of APS on lung adenocarcinoma A549 cells. The effects of APS and the anti-diabetic drug metformin
[...] Read more.
Astragalus polysaccharides (APSs), the compounds extracted from the common herb Astragalus membranaceus, have been extensively studied for their antitumor properties. In this study, we investigated the effect of APS on lung adenocarcinoma A549 cells. The effects of APS and the anti-diabetic drug metformin on apoptosis and ferroptosis were compared. Furthermore, the combination treatment of APS and metformin was also investigated. We found that APS not only reduced the growth of lung cancer cells but also had a synergistic effect with metformin on A549 cells. The study results showed that it may be promising to use APS and metformin as a combination therapy for the treatment of lung adenocarcinoma.
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(This article belongs to the Section Molecular Plant Sciences)
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Open AccessReview
Roles of SMAD and SMAD-Associated Signaling Pathways in Nerve Regeneration Following Peripheral Nerve Injury: A Narrative Literature Review
by
Jeongmin Lee, Dong Keon Yon, Yong Sung Choi, Jinseok Lee, Joon Hyung Yeo, Sung Soo Kim, Jae Min Lee and Seung Geun Yeo
Curr. Issues Mol. Biol. 2024, 46(7), 7769-7781; https://doi.org/10.3390/cimb46070460 - 22 Jul 2024
Abstract
Although several methods are being applied to treat peripheral nerve injury, a perfect treatment that leads to full functional recovery has not yet been developed. SMAD (Suppressor of Mothers Against Decapentaplegic Homolog) plays a crucial role in nerve regeneration by facilitating the survival
[...] Read more.
Although several methods are being applied to treat peripheral nerve injury, a perfect treatment that leads to full functional recovery has not yet been developed. SMAD (Suppressor of Mothers Against Decapentaplegic Homolog) plays a crucial role in nerve regeneration by facilitating the survival and growth of nerve cells following peripheral nerve injury. We conducted a systematic literature review on the role of SMAD in this context. Following peripheral nerve injury, there was an increase in the expression of SMAD1, -2, -4, -5, and -8, while SMAD5, -6, and -7 showed no significant changes; SMAD8 expression was decreased. Specifically, SMAD1 and SMAD4 were found to promote nerve regeneration, whereas SMAD2 and SMAD6 inhibited it. SMAD exerts its effects by promoting neuronal survival and growth through BMP/SMAD1, BMP/SMAD4, and BMP/SMAD7 signaling pathways. Furthermore, it activates nerve regeneration programs via the PI3K/GSK3/SMAD1 pathway, facilitating active regeneration of nerve cells and subsequent functional recovery after peripheral nerve damage. By leveraging these mechanisms of SMAD, novel strategies for treating peripheral nerve damage could potentially be developed. We aim to further elucidate the precise mechanisms of nerve regeneration mediated by SMAD and explore the potential for developing targeted nerve treatments based on these findings.
Full article
(This article belongs to the Section Molecular Medicine)
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Open AccessArticle
Serum Extracellular Vesicles Cargo Approach in Bitches with Mammary Tumors
by
Gabriela C. Sousa, Marcos G. Carvalho, Carlos E. Fonseca-Alves and Fabiana F. Souza
Curr. Issues Mol. Biol. 2024, 46(7), 7745-7768; https://doi.org/10.3390/cimb46070459 - 22 Jul 2024
Abstract
This study investigated serum extracellular vesicles (EVs) in bitches with mammary neoplasms, in order to understand their size, shape, and concentration, as well as their association with tumor malignancy. Thirty bitches were categorized into control (n = 10), mammary tumor grades I
[...] Read more.
This study investigated serum extracellular vesicles (EVs) in bitches with mammary neoplasms, in order to understand their size, shape, and concentration, as well as their association with tumor malignancy. Thirty bitches were categorized into control (n = 10), mammary tumor grades I and II (GI, n = 13), and grade III (GII, n = 7). Serum was separated from blood collected during mastectomy, and EVs were isolated using size exclusion chromatography. The analysis revealed no significant differences in EV concentrations among groups, with similar concentrations for control, GI, and GII. Ninety-one proteins were identified in EV-enriched samples, with six showing varied abundance across groups. Notably, keratin 18 was highly abundant in GI, while sushi domain-containing protein, EvC ciliary subunit 2, and the joining chain of multimeric IgM and IgA were increased in GII. Additionally, protocadherin 17 and albumin were upregulated in both GI and GII. ROC curves identified potential biomarkers for differentiating tumor grades. Enrichment pathway analysis revealed AFP gene upregulation in the GI. Mass spectrometry proteomics data were deposited in Mendeley Data. The study provides valuable insights into serum EV characterization in bitches, suggesting keratin 18 and protocadherin 17 as potential biomarkers for canine mammary neoplasia, with implications for future diagnostic and therapeutic strategies.
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(This article belongs to the Special Issue Targeting Tumor Microenvironment for Cancer Therapy, 2nd Edition)
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Open AccessArticle
Downregulation of Splicing Factor PTBP1 Curtails FBXO5 Expression to Promote Cellular Senescence in Lung Adenocarcinoma
by
Haoyu Li, Xiaoxiao Sun, Yuanyuan Lv, Gang Wei, Ting Ni, Wenxin Qin, Haojie Jin and Qi Jia
Curr. Issues Mol. Biol. 2024, 46(7), 7730-7744; https://doi.org/10.3390/cimb46070458 - 19 Jul 2024
Abstract
Polypyrimidine tract-binding protein 1 (PTBP1) plays an essential role in splicing and post-transcriptional regulation. Moreover, PTBP1 has been implicated as a causal factor in tumorigenesis. However, the involvement of PTBP1 in cellular senescence, a key biological process in aging and cancer
[...] Read more.
Polypyrimidine tract-binding protein 1 (PTBP1) plays an essential role in splicing and post-transcriptional regulation. Moreover, PTBP1 has been implicated as a causal factor in tumorigenesis. However, the involvement of PTBP1 in cellular senescence, a key biological process in aging and cancer suppression, remains to be clarified. Here, it is shown that PTBP1 is associated with the facilitation of tumor growth and the prognosis in lung adenocarcinoma (LUAD). PTBP1 exhibited significantly increased expression in various cancer types including LUAD and showed consistently decreased expression in multiple cellular senescence models. Suppression of PTBP1 induced cellular senescence in LUAD cells. In terms of molecular mechanisms, the silencing of PTBP1 enhanced the skipping of exon 3 in F-box protein 5 (FBXO5), resulting in the generation of a less stable RNA splice variant, FBXO5-S, which subsequently reduces the overall FBXO5 expression. Additionally, downregulation of FBXO5 was found to induce senescence in LUAD. Collectively, these findings illustrate that PTBP1 possesses an oncogenic function in LUAD through inhibiting senescence, and that targeting aberrant splicing mediated by PTBP1 has therapeutic potential in cancer treatment.
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(This article belongs to the Special Issue RNA Sequencing Data Research on Ageing and Age-Related Diseases)
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