XXXX mediates autophagic cell death in renal proximal tubular cells.

@entity1 @entity8 @entity607 @entity10407 @entity8186 @entity740 @entity8783 @entity1178 @entity810 @entity35
UNASSIGNED: Higher serum level of @entity607 (PC) in @entity740 ( @entity740 ) @entity1 has been linked with @entity740 progression. The toxic effect of PC on diverse cells has been reported by prior studies, except for renal tubular cells. Both autophagy and apoptosis contribute to renal tubular cell death, yet evidence of its response to PC is limited and their crosstalk is still unclear. Autophagy is an important cellular process involved in toxin-induced cell death. @entity8 in @entity810 is thought to be one of the key events causing the progression of @entity740 . Thus, we treated @entity35 (NRK-52E) and @entity1 (HRPTEC) renal proximal tubular cells (RPTC) with PC and found the cell proliferation was significantly decreased. Cell apoptosis was significantly increased and accompanied with the activation of autophagy as evidenced by increases in LC3-II, @entity8783 and Atg 4. We also found an increase of @entity10407 by @entity1178 activation. @entity10407 accumulation could mediate the activation of @entity8186 -dependent cell apoptosis. Conversely, knockdown of @entity10407 by siRNA of @entity10407 had the opposite effect by arresting LC3-II accumulation and promoting increasing cell viability. We conclude that PC triggered autophagic RPTC death via JNK-mediated @entity10407 accumulation and then activated @entity8186 -dependent cell death pathway. PC can be considered as one of the key events causing progression of @entity740 , which might affect drug disposition in @entity740 cases.
