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

Research output: Contribution to journalArticle

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

Related Edinburgh Organisations

Original languageEnglish
Pages (from-to)1310-20
Number of pages11
JournalEndocrinology
Volume154
Issue number3
DOIs
Publication statusPublished - Mar 2013

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.

    Research areas

  • Aging, Animals, Cell Count, Follistatin-Related Proteins, Ligands, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Organ Size, Proteins, Proto-Oncogene Proteins c-akt, Sertoli Cells, Signal Transduction, Sirtuin 1, Spermatogenesis, Testis, Transforming Growth Factor beta

ID: 24527643