Follistatin-like 3 (FSTL3) mediated silencing of transforming growth factor β (tgfβ) signaling is essential for testicular aging and regulating testis size

Karla J. Oldknow, Jan Seebacher, Tapasree Goswami, Judit Villen, Andrew A. Pitsillides, Peter J. O'Shaughnessy, Steven P. Gygi, Alan L. Schneyer, Abir Mukherjee

Research output: Contribution to journalArticlepeer-review

36 Citations (Scopus)

Abstract

Follistatin-like 3 (FSTL3) is a glycoprotein that binds and inhibits the action of TGFβ ligands such as activin. The roles played by FSTL3 and activin signaling in organ development and homeostasis are not fully understood. The authors show mice deficient in FSTL3 develop markedly enlarged testes that are also delayed in their age-related regression. These FSTL3 knockout mice exhibit increased Sertoli cell numbers, allowing for increased spermatogenesis but otherwise showing normal testicular function. The data show that FSTL3 deletion leads to increased AKT signaling and SIRT1 expression in the testis. This demonstrates a cross-talk between TGFβ ligand and AKT signaling and leads to a potential mechanism for increased cellular survival and antiaging. The findings identify crucial roles for FSTL3 in limiting testis organ size and promoting age-related testicular regression. Copyright © 2013 by The Endocrine Society.
Original languageEnglish
Pages (from-to)1310-1320
Number of pages11
JournalEndocrinology
Volume154
Issue number3
DOIs
Publication statusPrint publication - 1 Mar 2013
Externally publishedYes

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