ArticleCellular and molecular life sciences : CMLS2022
Sertoli cell survival and barrier function are regulated by miR-181c/d-Pafah1b1 axis during mammalian spermatogenesis.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- Bta-miR-146a Inhibits Proliferation and Promotes Apoptosis of Bovine Immature Sertoli Cells by Targeting SMAD4 via the TGF-β/MAPK Signaling Pathway.International journal of molecular sciences · 2026Article
- miR-124 Ameliorates Spatial Memory Deficits in Rats Exposed to Single-Prolonged Stress by Downregulating IQGAP1 to Regulate Actin-Binding Proteins and Apoptosis in Hippocampal Neurons.Molecular neurobiology · 2026Article
- Gut microbiota induces dysspermatogenesis via microbial-derived phenylacetylglycine in Ggt1-deficient mice.Microbiome · 2026Article
- miRNA Sequencing and Differential Analysis of Testes from 1-Year-Old and 3-Year-Old Kazakh Horses.Biology · 2026Article
- Dual-Phase Immunomodulation by the Bovine β-Casein Peptide KEMPFPK: Insights into Potential TLR Interaction and Gut Microbiota-Mediated Effects.Foods (Basel, Switzerland) · 2026Article
- Article
- Methionine deficiency causes spermatogonial apoptosis via oxidative stress and DNA damage response pathway.Biological research · 2025Article
- [Research progress on glycolipid metabolism of Sertoli cell in the development of spermatogenic cell].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025Review
- The microRNA-mediated apoptotic signaling axis in male reproduction: a possible and targetable culprit in male infertility.Cell biology and toxicology · 2025Review
- IQ motif family genes in male infertility: pathogenesis, mechanisms, and clinical perspectives.Frontiers in reproductive health · 2025Review
- DCAF2 regulates the proliferation and differentiation of mouse progenitor spermatogonia by targeting p21 and thymine DNA glycosylase.Cell proliferation · 2024Article
- Inhibition ofCells · 2024Article
- MicroRNAs in spermatogenesis dysfunction and male infertility: clinical phenotypes, mechanisms and potential diagnostic biomarkers.Frontiers in endocrinology · 2024Review
- The Role of microRNA in Spermatogenesis: Is There a Place for Fertility Preservation Innovation?International journal of molecular sciences · 2023Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Sertoli cells contribute to the formation of the blood-testis barrier (BTB), which is necessary for normal spermatogenesis. Recently, microRNAs (miRNAs) have emerged as posttranscriptional regulatory elements in BTB function during spermatogenesis. Our previous study has shown that miR-181c or miR-181d (miR-181c/d) is highly expressed in testes from boars at 60 days old compared with at 180 days old. Herein, we found that overexpression of miR-181c/d via miR-181c/d mimics in murine Sertoli cells (SCs) or through injecting miR-181c/d-overexpressing lentivirus in murine testes perturbs BTB function by altering BTB-associated protein distribution at the Sertoli cell-cell interface and F-actin organization, but this in vivo perturbation disappears approximately 6 weeks after the final treatment. We also found that miR-181c/d represses Sertoli cell proliferation and promotes its apoptosis. Moreover, miR-181c/d regulates Sertoli cell survival and barrier function by targeting platelet-activating factor acetylhydrolase 1b regulatory subunit 1 (Pafah1b1) gene. Furthermore, miR-181c/d suppresses PAFAH1B1 expression, reduces the complex of PAFAH1B1 with IQ motif-containing GTPase activating protein 1, and inhibits CDC42/PAK1/LIMK1/Cofilin pathway which is required for F-actin stabilization. In total, our results reveal the regulatory axis of miR-181c/d-Pafah1b1 in cell survival and barrier function of Sertoli cells and provide additional insights into miRNA functions in mammalian spermatogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.