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MicroRNA Regulation in Human Health and Diseases
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MicroRNA Regulation in Human Health and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 February 2025) | Viewed by 7139

Special Issue Editor

Dr. Rachel E. Crossland

E-Mail Website
Guest Editor
Translational and Clinical Research Institute, Newcastle University, Newcastle NE2 4HH, UK
Interests: microRNA; GvHD; exosome; extracellular vesicle; transplantation

Special Issue Information

Dear Colleagues,

MicroRNAs are a class of non-coding small RNAs, approximately 19–22 nucleotides in length, that functionally target mRNA via a small seed sequence to post-transcriptionally regulate gene expression. They play a fundamental role in major cellular functions such as development, differentiation, growth, and metabolism. To date, over 2000 microRNA species have been identified, and our knowledge of their biological functions, biogenesis, and targeting has grown exponentially. In addition to their role in normal biological processes, microRNAs have been linked to the development of numerous diseases, ranging from metabolic and inflammatory diseases to malignancy. More recently, microRNAs have been shown to be present in biofluids, where they are protected from RNase-mediated degradation by encapsulation into extracellular vesicles (EVs), or through binding to protective proteins. This has paved the way for the intense exploration of their potential as circulatory biomarkers and novel therapeutics or drug delivery vehicles. However, despite intense research, many questions remain the focus of investigation, including but not limited to the following:

  • Mechanisms of microRNA action during pathological processes and disease;
  • MicroRNA-based therapeutics, delivery systems and their clinical application;
  • MicroRNA biomarkers, including circulatory microRNAs;
  • The role of microRNAs in cell-to-cell communication;
  • The extracellular function of microRNAs in both health and disease;
  • MicroRNA signalling pathways;
  • MicroRNA target identification.

Dr. Rachel E. Crossland
Guest Editor

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

  • microRNA
  • biomarkers
  • extracellular vesicle
  • intercellular communication
  • signalling
  • therapeutics

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Published Papers (5 papers)

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Research

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13 pages, 3770 KiB  
Article
Tuberculous Pleural Effusion-Derived Exosomal miR-130b-3p and miR-423-5p Promote the Proliferation of Lung Cancer Cells via Cyclin D1
by Hyun-Jung Kang, Sangho Yun, Seung-Ho Shin, Dong Hyuk Youn, Ga-Hyun Son, Jae Jun Lee and Ji Young Hong
Int. J. Mol. Sci. 2024, 25(18), 10119; https://doi.org/10.3390/ijms251810119 - 20 Sep 2024
Cited by 1 | Viewed by 1187
Abstract
Epidemiologic studies have shown an association between tuberculosis and lung cancer. The altered tumor microenvironment after tuberculosis infection appears to contribute to cancer progression. Pleural effusions are enriched in exosomes, which act as mediators of intercellular communication. We hypothesized that tuberculous pleural effusion [...] Read more.
Epidemiologic studies have shown an association between tuberculosis and lung cancer. The altered tumor microenvironment after tuberculosis infection appears to contribute to cancer progression. Pleural effusions are enriched in exosomes, which act as mediators of intercellular communication. We hypothesized that tuberculous pleural effusion (TPE)-derived exosomes mediate intercellular communication. Then, we examined the interaction between TPE-derived exosomes and cancer cells. Exosomal miRNA profiling of TPE was performed using a microRNA array. An in vitro lung cancer cell experiment and an in vivo mouse xenograft tumor model were used to evaluate the effects of the selected exosomal microRNAs. TPE-derived exosome treatment enhanced the growth of A549 cells both in vitro and in a nude mouse xenograft model. Neighboring cancer cells were observed to take up TPE-derived exosomes, which promoted cancer cell invasion. Exosome-mediated transfer of the selected microRNAs, including miR-130b-3p and miR-423-5p, to A549 lung cancer cells activated cyclin D1 signaling and increased the expression of phosphorylated p65, a cyclin D1 transcription factor. Inhibitors of miR-130b and miR-423-5p suppressed the promotion of lung cancer by TPE-derived exosomes and reduced the expression of p65 and cyclin D1. These results suggest that TPE-derived exosomal miRNAs can serve as a novel therapeutic target in tuberculous fibrosis-induced lung cancer. Full article
(This article belongs to the Special Issue MicroRNA Regulation in Human Health and Diseases)
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16 pages, 4651 KiB  
Article
MicroRNA-27a-5p Downregulates Expression of Proinflammatory Cytokines in Lipopolysaccharide-Stimulated Human Dental Pulp Cells via the NF-κB Signaling Pathway
by Shihan Wang, Nobuyuki Kawashima, Peifeng Han, Keisuke Sunada-Nara, Ziniu Yu, Kento Tazawa, Mayuko Fujii, Thoai Quoc Kieu and Takashi Okiji
Int. J. Mol. Sci. 2024, 25(17), 9694; https://doi.org/10.3390/ijms25179694 - 7 Sep 2024
Cited by 4 | Viewed by 1148
Abstract
MicroRNA-27a-5p (miR-27a-5p) was significantly upregulated in dental pulp inflammation, yet its underlying mechanisms remain unclear. This study investigated the effect of miR-27a-5p on the expression of proinflammatory cytokines in human dental pulp cells (hDPCs) stimulated by lipopolysaccharide (LPS). LPS-stimulated hDPCs showed concurrent increases [...] Read more.
MicroRNA-27a-5p (miR-27a-5p) was significantly upregulated in dental pulp inflammation, yet its underlying mechanisms remain unclear. This study investigated the effect of miR-27a-5p on the expression of proinflammatory cytokines in human dental pulp cells (hDPCs) stimulated by lipopolysaccharide (LPS). LPS-stimulated hDPCs showed concurrent increases in the expression of miR-27a-5p and proinflammatory cytokines (IL-6, IL-8, and MCP1), and the increased expression was suppressed by NF-κB inhibitor BAY 11-0785. Transfection of the miR-27a-5p mimic downregulated the expression of proinflammatory cytokines, NF-κB activity, and the expression of NF-κB signaling activators (TAB1, IRAK4, RELA, and FSTL1) in LPS-stimulated hDPCs. Luciferase reporter assays revealed that miR-27a-5p bound directly to the 3’-UTR of TAB1. siTAB1 downregulated NF-κB activity and proinflammatory cytokine expression. Downregulation of proinflammatory cytokine expression, NF-κB activity, and NF-κB signaling activator expression (TAB1, IRAK4, and RELA) was also found in LPS-stimulated rat incisor pulp tissue explants following transfection with the miR-27a-5p mimic ex vivo. MiR-27a-5p, whose expression was induced by NF-κB signaling, negatively regulated the synthesis of proinflammatory cytokines via targeting NF-κB signaling. In particular, TAB1, a potent NF-κB activator, was targeted by miR-27a-5p. These results provide insights into the negative regulatory effects of miR-27a-5p, particularly those targeting the TAB1-NF-κB signaling pathway, on pulp inflammation. Full article
(This article belongs to the Special Issue MicroRNA Regulation in Human Health and Diseases)
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12 pages, 746 KiB  
Article
Involvement of Expression of miR33-5p and ABCA1 in Human Peripheral Blood Mononuclear Cells in Coronary Artery Disease
by Yazmín Estela Torres-Paz, Ricardo Gamboa, Giovanny Fuentevilla-Álvarez, Guillermo Cardoso-Saldaña, Rocío Martínez-Alvarado, María Elena Soto and Claudia Huesca-Gómez
Int. J. Mol. Sci. 2024, 25(16), 8605; https://doi.org/10.3390/ijms25168605 - 7 Aug 2024
Cited by 1 | Viewed by 1021
Abstract
MicroRNAs (miRs) are small non-coding RNAs that regulate gene expression post-transcriptionally and are crucial in lipid metabolism. ATP-binding cassette transporter A1 (ABCA1) is essential for cholesterol efflux from cells to high-density lipoprotein (HDL). Dysregulation of miRs targeting ABCA1 can affect cholesterol homeostasis and [...] Read more.
MicroRNAs (miRs) are small non-coding RNAs that regulate gene expression post-transcriptionally and are crucial in lipid metabolism. ATP-binding cassette transporter A1 (ABCA1) is essential for cholesterol efflux from cells to high-density lipoprotein (HDL). Dysregulation of miRs targeting ABCA1 can affect cholesterol homeostasis and contribute to coronary artery disease (CAD). This study aimed to investigate the expression of miRs targeting ABCA1 in human monocytes, their role in cholesterol efflux, and their relationship with CAD. We included 50 control and 50 CAD patients. RT-qPCR examined the expression of miR-33a-5p, miR-26a-5p, and miR-144-3p in monocytes. Logistic regression analysis explored the association between these miRs and CAD. HDL’s cholesterol acceptance was analyzed using the J774A.1 cell line. Results showed that miR-26a-5p (p = 0.027) and ABCA1 (p = 0.003) expression levels were higher in CAD patients, while miR-33a-5p (p < 0.001) levels were lower. Downregulation of miR-33a-5p and upregulation of ABCA1 were linked to a lower CAD risk. Atorvastatin upregulated ABCA1 mRNA, and metformin downregulated miR-26a-5p in CAD patients. Decreased cholesterol efflux correlated with higher CAD risk and inversely with miRs in controls. Reduced miR-33a-5p expression and increased ABCA1 expression are associated with decreased CAD risk. miR deregulation in monocytes may influence atherosclerotic plaque formation by regulating cholesterol efflux. Atorvastatin and metformin could offer protective effects by modulating miR-33a-5p, miR-26a-5p, and ABCA1, suggesting potential therapeutic strategies for CAD prognosis and treatment. Full article
(This article belongs to the Special Issue MicroRNA Regulation in Human Health and Diseases)
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23 pages, 3642 KiB  
Article
Dual Role of microRNA-146a in Experimental Inflammation in Human Pulmonary Epithelial and Immune Cells and Expression in Inflammatory Lung Diseases
by Lucia Gronau, Ruth P. Duecker, Silvija-Pera Jerkic, Olaf Eickmeier, Jordis Trischler, Andreas G. Chiocchetti, Katharina Blumchen, Stefan Zielen and Ralf Schubert
Int. J. Mol. Sci. 2024, 25(14), 7686; https://doi.org/10.3390/ijms25147686 - 13 Jul 2024
Cited by 2 | Viewed by 2207
Abstract
microRNA (miR)-146a emerges as a promising post-transcriptional regulator in various inflammatory diseases with different roles for the two isoforms miR-146a-5p and miR-146a-3p. The present study aimed to examine the dual role of miR-146a-5p and miR-146a 3p in the modulation of inflammation in human [...] Read more.
microRNA (miR)-146a emerges as a promising post-transcriptional regulator in various inflammatory diseases with different roles for the two isoforms miR-146a-5p and miR-146a-3p. The present study aimed to examine the dual role of miR-146a-5p and miR-146a 3p in the modulation of inflammation in human pulmonary epithelial and immune cells in vitro as well as their expression in patients with inflammatory lung diseases. Experimental inflammation in human A549, HL60, and THP1 via the NF-kB pathway resulted in the major upregulation of miR-146a-5p and miR-146a-3p expression, which was partly cell-specific. Modulation by transfection with miRNA mimics and inhibitors demonstrated an anti-inflammatory effect of miR-146a-5p and a pro-inflammatory effect of miR-146a-3p, respectively. A mutual interference between miR-146a-5p and miR-146a-3p was observed, with miR-146a-5p exerting a predominant influence. In vivo NGS analyses revealed an upregulation of miR-146a-3p in the blood of patients with cystic fibrosis and bronchiolitis obliterans, while miR-146a-5p levels were downregulated or unchanged compared to controls. The reverse pattern was observed in patients with SARS-CoV-2 infection. In conclusion, miR-146a-5p and miR-146a-3p are two distinct but interconnected miRNA isoforms with opposing functions in inflammation regulation. Understanding their interaction provides important insights into the progression and persistence of inflammatory lung diseases and might provide potential therapeutic options. Full article
(This article belongs to the Special Issue MicroRNA Regulation in Human Health and Diseases)
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Review

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32 pages, 747 KiB  
Review
Exploring the Role of microRNAs as Blood Biomarkers in Alzheimer’s Disease and Frontotemporal Dementia
by Irene Petracci, Sonia Bellini, Katarzyna Goljanek-Whysall, Leo R. Quinlan, Agnieszka Fiszer, Ali Cakmak, Cyrille Mesue Njume, Barbara Borroni and Roberta Ghidoni
Int. J. Mol. Sci. 2025, 26(7), 3399; https://doi.org/10.3390/ijms26073399 - 5 Apr 2025
Viewed by 485
Abstract
Alzheimer’s disease (AD) and frontotemporal dementia (FTD) are the most common forms of dementia globally. AD is characterized by the accumulation of amyloid-β (Aβ) plaques and hyperphosphorylated tau in the brain, leading to progressive memory loss and cognitive decline, significantly impairing daily life. [...] Read more.
Alzheimer’s disease (AD) and frontotemporal dementia (FTD) are the most common forms of dementia globally. AD is characterized by the accumulation of amyloid-β (Aβ) plaques and hyperphosphorylated tau in the brain, leading to progressive memory loss and cognitive decline, significantly impairing daily life. In contrast, FTD is marked by selective degeneration of the frontal and/or temporal lobes, typically resulting in profound changes in personality and social behavior, speech disorders, and psychiatric symptoms. Numerous studies have found microRNAs (miRNAs)—small, non-coding RNA molecules that regulate gene expression post-transcriptionally—to be dysregulated in AD and FTD. As a result, miRNAs have emerged as promising novel biomarkers for these diseases. This review examines the current understanding of miRNAs in AD and FTD, emphasizing their potential as accessible, noninvasive biomarkers for diagnosing these prevalent neurodegenerative disorders. Full article
(This article belongs to the Special Issue MicroRNA Regulation in Human Health and Diseases)
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