Activation of Toll like receptor 3 induces spermatogonial stem cell apoptosis. (9th September 2015)

• Record Type: Journal Article
• Authors: Hu, Jianxin; Song, Dalong; Luo, Guangheng; Xu, Suxiong; Cao, Ying; Sun, Zhaolin
• Is Part Of: Cell biochemistry and function. Volume 33:Number 6(2015:Aug.)
• Page Start: 415
• Page End: 422
• Publication Date: 2015-09-09
• Subjects: Cytochemistry -- Periodicals; Cell metabolism -- Periodicals; Biochemistry -- Periodicals; Cytology -- Periodicals; 572
• DOI: 10.1002/cbf.3133
• Languages: English
• ISSNs: 0263-6484

Abstract

<abstract abstract-type="main" id="cbf3133-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p id="cbf3133-para-0001">Germ cell apoptosis may be associated with the male infertility. The pathogenesis is to be further understood. Viral infection is one of the causative factors of apoptosis of the body cells. This study aims to investigate the role of activation of Toll like receptor (TLR)3 in the induction of germ cell apoptosis. In this study, spermatogonial stem cells (SSC) were isolated from C57BL/6 mouse testes. The expression of TLR3 on SSC was by RT‐qPCR and Western blotting. polyinosinic–polycytidylic acid (Poly I:C) was employed to activate TLR3 on SSCs. The results showed that re‐activation by PolyI:C induced SSC apoptosis. Exposure to PolyI:C induced interferon regulatory factor 3 (IRF3) phosphorylation in SSCs. TLR3 and IRF3 formed a complex in the SSCs. The complex of TLR3/IRF3 bound to the promoter of Fas ligand and promoted Fas ligand expression in SSC, and thus induced SSC apoptosis. In conclusion, the results of the present study indicate that activation of TLR3 by PolyI:C induces the SSC apoptosis, which implies that viral infection may interfere with the male germ cell development. Copyright © 2015 John Wiley &amp; Sons, Ltd.</p> </abstract>