CAMP signalling protects proximal tubular epithelial cells from cisplatin-induced apoptosis via activation of Epac.

ABSTRACT:

Background and purpose

Nephrotoxicity is the principal dose-limiting factor for cisplatin chemotherapy and is primarily associated with proximal tubular epithelial cells, including disruption of cell adhesions and induction of apoptosis. Cell adhesion and survival is regulated by, amongst other factors, the small GTPase Rap and its activator, the exchange protein directly activated by cAMP (Epac). Epac is particularly enriched in renal tubule epithelium. This study investigates the cytoprotective effects of cAMP-Epac-Rap signalling in a model of cisplatin-induced renal cell injury.

Experimental approach

The Epac-selective cAMP analogue 8-pCPT-2'-O-Me-cAMP was used to activate the Epac-Rap signalling pathway in proximal tubular epithelial cells. Cells were exposed to cisplati

SUBMITTER: Qin Y 

PROVIDER: S-EPMC3346244 | biostudies-literature | 2012 Feb

REPOSITORIES: biostudies-literature