Population Council Research that makes a difference

Abstract

TGF-β3 regulates the blood-testis barrier dynamics via the p38 mitogen activated protein (MAP) kinase pathway: An in vivo study (PDF) (HTML
Lui,Wing-Yee; Wong,Daria C.H.; Mruk,Dolores D.; Cheng,Chuen-yan
Endocrinology 144(4): 1139-1142
Publication date: 2003



Recent studies using Sertoli cells cultured in vitro to permittight junction (TJ) assembly have shown that TJ dynamics are regulated,at least in part, by TGF-ß3 via the p38 mitogen activated protein(MAP) kinase pathway. This in turn regulates the productionof occludin, a TJ-integral membrane protein, by Sertoli cells.Yet it is not known if this pathways is used by Sertoli cellsto regulate the blood-testis barrier (BTB) function in vivo.Using an in vivo model for studying BTB dynamics, we report hereinthe CdCl-induced BTB damage in rats was associated with a significantreduction in testicular occludin along with a loss of immunoreactiveoccludin in the seminiferous epithelium at the site of the BTB.Also, this CdCl-induced occludin loss from the BTB coincidedwith a surge in testicular TGF-ß3, as well as p-p38MAP kinase (the phosphorylated/activated form of p38), but notp38 MAP kinase and neither extracellular signal-regulated kinasenor its phosphorylated form (ERK/p-ERK), consistent with resultsof in vitro studies. More important, intratesticular administration ofSB202190, a specific p38 MAP kinase inhibitor, could block the CdCl-inducedoccludin loss from the BTB. These results illustrate that BTBdynamics in vivo are regulated by the TGF-ß3/p38 MAPkinase pathway, which in turn determines the level of occludinat the site of Sertoli cells TJs.




What's New

For 60 years, the Population Council has changed the way the world thinks about important health and development issues. Explore an interactive timeline of the Council's history, learn more about some of our key contributions, and watch a short video about why your support is so important to us.

Get Involved

Connect

  • Visit our Facebook page
  • Follow us on Twitter
  • Visit our Youtube channel