Objectives Recently there is accumulating evidence that the wnt/frizzled pathway may play a distinct role in cardiomyocytes apoptosis. We have demonstrated that staurosporine induces cardiomyocytes apoptosis in vitro. FrzA/sFRP-1, a secreted frizzled-related protein and antagonist for the wnt/frizzled pathway. This study was to explore the role of wnt/frizzled signalling pathway in staurosporine-induced apoptosis in cardiomyocytes and assessed the hypothesis that FrzA overexpression could attenuates staurosporine-induced apoptosis in cardiomyocytes.
Methods We found that the staurosporine induced the expression of Dvl-1 and subsequent up-regulation of b-catenin, which are the downstream members of wnt/frizzled pathway when cardiomyocytes apoptosis occurred. The staurosporine concentration elevated, apoptosis becomes serious and Dvl-1/b-catenin expression enhanced. Then cardiomyocytes were transfected with a recombinant AAV9 vector to deliver the FrzA gene, we found that FrzA gene suppression the expression of Dvl-1 and b-catenin and the activity of the Wnt/ frizzled pathway.
Results FrzA overexpression decreased the apoptotic rate, caspase-3 activity, and the Bax/Bcl-2 ratio in cardiomyocytes treated with staurosporine.
Conclusions Overexpression of FrzA inhibited the activity of the Wnt/frizzled pathway and reduced the apoptosis of cardiomyocytes.
Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.