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. Author manuscript; available in PMC: 2018 Sep 27.
Published in final edited form as: Circ Res. 2011 Mar 17;108(9):1102–1111. doi: 10.1161/CIRCRESAHA.110.229393

Figure 4. Depletion of μ-calpain with siRNA prevents upregulation of calpain activity in MMEC endothelial cells exposed to AngII.

Figure 4

Treatment of MMEC with siRNA to μ-calpain effectively reduces calpain expression levels (immunoblot). AngII fails to upregulates calpain activity in μ-calpain deficient MMEC (bar graph), thus demonstrating that the endothelial expressed μ-calpain isoform is the specific molecular target of AngII/AT1r signaling under our experimental conditions. AngII increases calpain activity via activation of the AT1r, as demonstrated by loss of increased calpain activity in MMEC treated with losartan. The calpain inhibitor ZLLal also prevented calpain activation in response to AngII. Calpain activity in attached MMEC was measured using a standard fluorescent assay and the calpain selective substrate T- Succ-LLVY-AMC. Numbers at the base of the bars indicate the number of independent experiments.