Integrin b4 in EMT: an implication of XXXX .

@entity1 @entity8 @entity82 @entity1075 @entity5962 @entity1970 @entity177 @entity2533 @entity5601 @entity12020
@entity8 is a main cause of @entity177 . Epithelial-to-mesenchymal transition (EMT) markers play a role in renal @entity82 . @entity2533 ( @entity2533 ) has been shown to initiate and complete the whole EMT process. It is now well accepted that loss of @entity5962 , EMT marker @entity1970 , and @entity12020 ( @entity12020 ) expression are key events in the EMT process. We found that by stimulating @entity1 renal proximal tubular epithelial ( @entity1 ) cells with @entity2533 , the expression of @entity5962 was down regulated and the expression of @entity1970 and @entity12020 were up regulated in a dose dependent manner. In our present study we also found that integrin @entity1075 ( @entity5601 -y) play roles in EMT process, with @entity2533 stimulation increasing integrin b4 expression in @entity1 cells. Integrin b4 and PPARy were detected in tubulointerstitial tissues, immunohistochemistry analysis showed enhanced expression of integrin b4 in early stage, with over-expression at later stage. In contrast, the expression of PPARy showed little increased in early stage, but was dramatically decreased at later stage. This is consistent with @entity2533 inducing EMT. Our immune-precipitation studies show that integrin b4 disassociation with PPARy is present in @entity5962 signaling. It suggests that PPARy has a role in EMT inhibition.
