AUTHOR=Ning Jin-zhuo , Li Wei , Cheng Fan , Yu Wei-min , Rao Ting , Ruan Yuan , Yuan Run , Zhang Xiao-bin , Zhuo Dong , Du Yang , Xiao Cheng-cheng 

TITLE=MiR-29a Suppresses Spermatogenic Cell Apoptosis in Testicular Ischemia-Reperfusion Injury by Targeting TRPV4 Channels

JOURNAL=Frontiers in Physiology

VOLUME=8

YEAR=2017

URL=https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2017.00966

DOI=10.3389/fphys.2017.00966

ISSN=1664-042X

ABSTRACT=<p><bold>Background:</bold> MicroRNAs (miRNAs) have emerged as gene expression regulators in the progression of ischemia-reperfusion injury (IRI). Accumulating evidences have indicated miR-29a play roles in myocardial and cerebral IRI. However, the role of miR-29a in testicular IRI has not been elucidated.</p><p><bold>Methods:</bold> Changes in expression of miR-29a and Transient Receptor Potential Vanilloid 4 (TRPV4) in animal samples and GC-1 spermatogenic cells were examined. The effects of miR-29a on spermatogenic cell apoptosis in testicular IRI were analyzed both <italic>in vitro</italic> and <italic>in vivo</italic>.</p><p><bold>Results:</bold> The expression of MiR-29a was negatively correlated with the expression of TRPV4 and significantly downregulated in animal samples and GC-1 cells as testicular IRI progressed. Further studies revealed TRPV4 as a downstream target of miR-29a. Inhibition of miR-29a expression increased the expression of TRPV4 and promoted spermatogenic cell apoptosis, whereas overexpression of miR-29a downregulated TRPV4 expression and suppressed spermatogenic cell apoptosis caused by testicular IRI <italic>in vitro</italic> and <italic>in vivo</italic>.</p><p><bold>Conclusion:</bold> Our results suggest that miR-29a suppresses apoptosis induced by testicular IRI by directly targeting TRPV4.</p>