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Cellular Signalling Transduction
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Cellular Signalling Transduction

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (15 August 2023) | Viewed by 12890

Special Issue Editors

Dr. Chiara Corrado

E-Mail Website
Guest Editor
Department of Biopathology and Medical Biotechnologies, University of Palermo, 90133 Palermo, Italy
Interests: extracellular vesicles; miRNA and Hypoxia; transduction signaling
Dr. Simona Fontana

E-Mail Website
Guest Editor
Department of Biopathology and Medical Biotechnologies, University of Palermo, 90133 Palermo, Italy
Interests: exosomes; extracellular vesicles; MicroRNA

Special Issue Information

Dear Colleagues,

It is well known that physiologically cells need to communicate with those around them and respond appropriately to the stimuli of the microenvironment.

Signal transduction is a complex process that involves the passage of information along signaling pathways involving different proteins that undergo, during the process, conformational changes important for their activity.

The first event of pathological conditions, such as neoplasia as well as neurological, immunogenic, or cardiac pathologies, is the alteration of this condition that finally determine a qualitatively and quantitatively altered downstream signaling.

An understanding of cellular transduction pathways will be helpful to clarify the evolution of a pathological condition and the subtle balance that regulates cellular homeostasis.

The Special Issue focuses on recent studies and clinical submissions with biomolecular experiments to have a more complete comprehension of cellular transduction signaling in physiological and pathological conditions, considering all the aspects of this complex puzzle.

Dr. Chiara Corrado
Dr. Simona Fontana
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • intracellular signalling transduction
  • cellular homeostasis
  • protein activity
  • cell–cell communication

Published Papers (6 papers)

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Research

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19 pages, 5468 KiB  
Article
Smad3 Mediates Diabetic Dyslipidemia and Fatty Liver in db/db Mice by Targeting PPARδ
by Huijun He, Yu Zhong, Honglian Wang, Patrick Ming-Kuen Tang, Vivian Weiwen Xue, Xiaocui Chen, Jiaoyi Chen, Xiaoru Huang, Cheng Wang and Huiyao Lan
Int. J. Mol. Sci. 2023, 24(14), 11396; https://doi.org/10.3390/ijms241411396 - 13 Jul 2023
Cited by 2 | Viewed by 1455
Abstract
Transforming growth factor-β (TGF-β)/Smad3 signaling has been shown to play important roles in fibrotic and inflammatory diseases. However, the role of Smad3 in dyslipidemia and non-alcoholic fatty liver disease (NAFLD) in type 2 diabetes remains unclear, and whether targeting Smad3 has a therapeutic [...] Read more.
Transforming growth factor-β (TGF-β)/Smad3 signaling has been shown to play important roles in fibrotic and inflammatory diseases. However, the role of Smad3 in dyslipidemia and non-alcoholic fatty liver disease (NAFLD) in type 2 diabetes remains unclear, and whether targeting Smad3 has a therapeutic effect on these metabolic abnormalities remains unexplored. These topics were investigated in this study in Smad3 knockout (KO)-db/db mice and by treating db/db mice with a Smad3-specific inhibitor SIS3. Compared to Smad3 wild-type (WT)-db/db mice, Smad3 KO-db/db mice were protected against dyslipidemia and NAFLD. Similarly, treatment of db/db mice with SIS3 at week 4 before the onset of type 2 diabetes until week 12 was capable of lowering blood glucose levels and improving diabetic dyslipidemia and NAFLD. In addition, using RNA-sequencing, the potential Smad3-target genes related to lipid metabolism was identified in the liver tissues of Smad3 KO/WT mice, and the regulatory mechanisms were investigated. Mechanistically, we uncovered that Smad3 targeted peroxisome proliferator-activated receptor delta (PPARδ) to induce dyslipidemia and NAFLD in db/db mice, which was improved by genetically deleting and pharmacologically inhibiting Smad3. Full article
(This article belongs to the Special Issue Cellular Signalling Transduction)
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15 pages, 2640 KiB  
Article
B-Cell Receptor Signaling Is Thought to Be a Bridge between Primary Sjogren Syndrome and Diffuse Large B-Cell Lymphoma
by Leila Mohammadnezhad, Mojtaba Shekarkar Azgomi, Marco Pio La Manna, Giuliana Guggino, Cirino Botta, Francesco Dieli and Nadia Caccamo
Int. J. Mol. Sci. 2023, 24(9), 8385; https://doi.org/10.3390/ijms24098385 - 7 May 2023
Cited by 1 | Viewed by 1702
Abstract
Primary Sjogren syndrome (pSS) is the second most common autoimmune disorder worldwide, which, in the worst scenario, progresses to Non-Hodgkin Lymphoma (NHL). Despite extensive studies, there is still a lack of knowledge about developing pSS for NHL. This study focused on cells’ signaling [...] Read more.
Primary Sjogren syndrome (pSS) is the second most common autoimmune disorder worldwide, which, in the worst scenario, progresses to Non-Hodgkin Lymphoma (NHL). Despite extensive studies, there is still a lack of knowledge about developing pSS for NHL. This study focused on cells’ signaling in pSS progression to the NHL type of diffuse large B-cell lymphoma (DLBCL). Using bulk RNA and single cell analysis, we found five novel pathologic-independent clusters in DLBCL based on cells’ signaling. B-cell receptor (BCR) signaling was identified as the only enriched signal in DLBCL and pSS peripheral naive B-cells or salivary gland-infiltrated cells. The evaluation of the genes in association with BCR has revealed that targeting CD79A, CD79B, and LAMTOR4 as the shared genes can provide novel biomarkers for pSS progression into lymphoma. Full article
(This article belongs to the Special Issue Cellular Signalling Transduction)
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14 pages, 1596 KiB  
Article
Expression of Non-T Cell Activation Linker (NTAL) in Jurkat Cells Negatively Regulates TCR Signaling: Potential Role in Rheumatoid Arthritis
by Isaac Narbona-Sánchez, Alba Pérez-Linaza, Isabel Serrano-García, Inmaculada Vico-Barranco, Luis M. Fernández-Aguilar, José L. Poveda-Díaz, María J. Sánchez del Pino, Fermín Medina-Varo, Mikel M. Arbulo-Echevarria and Enrique Aguado
Int. J. Mol. Sci. 2023, 24(5), 4574; https://doi.org/10.3390/ijms24054574 - 26 Feb 2023
Cited by 1 | Viewed by 1693
Abstract
T lymphocytes are key players in adaptive immune responses through the recognition of peptide antigens through the T Cell Receptor (TCR). After TCR engagement, a signaling cascade is activated, leading to T cell activation, proliferation, and differentiation into effector cells. Delicate control of [...] Read more.
T lymphocytes are key players in adaptive immune responses through the recognition of peptide antigens through the T Cell Receptor (TCR). After TCR engagement, a signaling cascade is activated, leading to T cell activation, proliferation, and differentiation into effector cells. Delicate control of activation signals coupled to the TCR is needed to avoid uncontrolled immune responses involving T cells. It has been previously shown that mice deficient in the expression of the adaptor NTAL (Non-T cell activation linker), a molecule structurally and evolutionarily related to the transmembrane adaptor LAT (Linker for the Activation of T cells), develop an autoimmune syndrome characterized by the presence of autoantibodies and enlarged spleens. In the present work we intended to deepen investigation into the negative regulatory functions of the NTAL adaptor in T cells and its potential relationship with autoimmune disorders. For this purpose, in this work we used Jurkat cells as a T cell model, and we lentivirally transfected them to express the NTAL adaptor in order to analyze the effect on intracellular signals associated with the TCR. In addition, we analyzed the expression of NTAL in primary CD4+ T cells from healthy donors and Rheumatoid Arthritis (RA) patients. Our results showed that NTAL expression in Jurkat cells decreased calcium fluxes and PLC-γ1 activation upon stimulation through the TCR complex. Moreover, we showed that NTAL was also expressed in activated human CD4+ T cells, and that the increase of its expression was reduced in CD4+ T cells from RA patients. Our results, together with previous reports, suggest a relevant role for the NTAL adaptor as a negative regulator of early intracellular TCR signaling, with a potential implication in RA. Full article
(This article belongs to the Special Issue Cellular Signalling Transduction)
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25 pages, 6077 KiB  
Article
Neuromedin S Regulates Steroidogenesis through Maintaining Mitochondrial Morphology and Function via NMUR2 in Goat Ovarian Granulosa Cells
by Xuan Sun, Cheng Zeng, Feng Wang, Zhen Zhang, Fan Yang, Zhi-Peng Liu, Kang Li and Guo-Min Zhang
Int. J. Mol. Sci. 2022, 23(21), 13402; https://doi.org/10.3390/ijms232113402 - 2 Nov 2022
Cited by 5 | Viewed by 1538
Abstract
Neuromedin S (NMS) plays various roles in reproductive regulation, while the mechanism by which NMS regulates ovarian steroidogenesis remains unclear. In the current study, we confirmed the enhancement role of NMS in steroidogenesis in goat ovarian granulosa cells (GCs). To further explore the [...] Read more.
Neuromedin S (NMS) plays various roles in reproductive regulation, while the mechanism by which NMS regulates ovarian steroidogenesis remains unclear. In the current study, we confirmed the enhancement role of NMS in steroidogenesis in goat ovarian granulosa cells (GCs). To further explore the specific mechanism, we conducted a knockdown of NMUR2 in GCs followed by treatment with NMS and determined the effects of NMS treatment on mitochondrial morphology and function. The results found that NMS treatment increased the production of estrogen and up-regulated the expression of STAR, CYP11A1, 3BHSD, and CYP19A1, while the effects of NMS treatment were blocked by the knockdown of NMUR2 in goat GCs. Moreover, NMS treatment enhanced the fusion of mitochondria and up-regulated the expression of OPA1, MFN1, and MFN2, and increased mitochondrial membrane potential, the activity of respiratory chain enzymes and ATP production by maintaining a low expression level of mitochondrial unfolded protein response markers. The effects of NMS treatment on mitochondria were reversed by NMUR2 knockdown and NMS cotreatment. The possible mechanism of the results above was revealed by NMS treatment activating the Hippo pathway effector YAP1 and then managing the expression of phosphorylation PPARGC1A (Ser571). Together, these data showed that NMS promoted the fusion of mitochondria and protected mitochondrial function from mitochondrial unfolded protein response possibly via the NMUR2/YAP1/PPARGC1A pathway, thereby affecting the steroidogenesis of goat GCs. By elaborating the potential mechanism of NMS in regulating estrogen production in goat GCs, our results can serve as the mechanism reference for follicular growth and development. Full article
(This article belongs to the Special Issue Cellular Signalling Transduction)
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Review

Jump to: Research

18 pages, 1715 KiB  
Review
The Multifunctional Protein Syntenin-1: Regulator of Exosome Biogenesis, Cellular Function, and Tumor Progression
by Kwang-Min Lee, Eun-Chan Seo, Jeong-Hyung Lee, Hyo-Jin Kim and Cheol Hwangbo
Int. J. Mol. Sci. 2023, 24(11), 9418; https://doi.org/10.3390/ijms24119418 - 29 May 2023
Cited by 3 | Viewed by 2970
Abstract
Syntenin acts as an adaptor and scaffold protein through its two PSD-95, Dlg, and ZO-1 (PDZ) domains, participating in multiple signaling pathways and modulating cellular physiology. It has been identified as an oncogene, promoting cancer development, metastasis, and angiogenesis in various carcinomas. Syntenin-1 [...] Read more.
Syntenin acts as an adaptor and scaffold protein through its two PSD-95, Dlg, and ZO-1 (PDZ) domains, participating in multiple signaling pathways and modulating cellular physiology. It has been identified as an oncogene, promoting cancer development, metastasis, and angiogenesis in various carcinomas. Syntenin-1 is also associated with the production and release of exosomes, small extracellular vesicles that play a significant role in intercellular communication by containing bioactive molecules such as proteins, lipids, and nucleic acids. The trafficking of exosomes involves a complex interplay of various regulatory proteins, including syntenin-1, which interacts with its binding partners, syndecan and activated leukocyte cell adhesion molecule (ALIX). Exosomal transfer of microRNAs, a key cargo, can regulate the expression of various cancer-related genes, including syntenin-1. Targeting the mechanism involving the regulation of exosomes by syntenin-1 and microRNAs may provide a novel treatment strategy for cancer. This review highlights the current understanding of syntenin-1’s role in regulating exosome trafficking and its associated cellular signaling pathways. Full article
(This article belongs to the Special Issue Cellular Signalling Transduction)
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21 pages, 1798 KiB  
Review
Effects of Flavonoids on Cancer, Cardiovascular and Neurodegenerative Diseases: Role of NF-κB Signaling Pathway
by Maria Magdalena Barreca, Riccardo Alessandro and Chiara Corrado
Int. J. Mol. Sci. 2023, 24(11), 9236; https://doi.org/10.3390/ijms24119236 - 25 May 2023
Cited by 7 | Viewed by 2663
Abstract
Flavonoids are polyphenolic phytochemical compounds found in many plants, fruits, vegetables, and leaves. They have a multitude of medicinal applications due to their anti-inflammatory, antioxidative, antiviral, and anticarcinogenic properties. Furthermore, they also have neuroprotective and cardioprotective effects. Their biological properties depend on the [...] Read more.
Flavonoids are polyphenolic phytochemical compounds found in many plants, fruits, vegetables, and leaves. They have a multitude of medicinal applications due to their anti-inflammatory, antioxidative, antiviral, and anticarcinogenic properties. Furthermore, they also have neuroprotective and cardioprotective effects. Their biological properties depend on the chemical structure of flavonoids, their mechanism of action, and their bioavailability. The beneficial effects of flavonoids have been proven for a variety of diseases. In the last few years, it is demonstrated that the effects of flavonoids are mediated by inhibiting the NF-κB (Nuclear Factor-κB) pathway. In this review, we have summarized the effects of some flavonoids on the most common diseases, such as cancer, cardiovascular, and human neurodegenerative diseases. Here, we collected all recent studies describing the protective and prevention role of flavonoids derived from plants by specifically focusing their action on the NF-κB signaling pathway. Full article
(This article belongs to the Special Issue Cellular Signalling Transduction)
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