Molecular Mechanism of HSF1-Upregulated ALDH2 by PKC in Ameliorating Pressure Overload-Induced Heart Failure in Mice

Figure 4

The expression of HSF1, PKC, ALDH2, HSP90, and beta-MHC in upregulated or downregulated HSF1 mouse heart tissue or cardiomyocytes. (a) The protein level of PKC and HSF90 in the WT, HSF1 TG, and HSF1 KO mouse heart tissues after TAC for 4 weeks. (sham: sham-operated mice; WT: wild-type mice; HSF1 TG: HSF1 transgene mice; HSF1 KO: HSF1 knockout mice). (b) The protein level of HSF1, HSP90, and PKC in upregulated or downregulated HSF1 cardiomyocytes. (control: cardiomyocytes without mechanical stretch; MS: cardiomyocytes with mechanical stretch 48 h; Ad-HSF1-shRNA+MS: cardiomyocytes infected by adenovirus-expressing HSF1 shRNA with mechanical stretch 48 h; Ad-HSF1+MS: cardiomyocytes infected by adenovirus-expressing HSF1 with mechanical stretch 48 h). (c) The expression of HSF1, PKC, ALDH2, and beta-MHC in upregulated HSF1 cardiomyocytes (MS: cardiomyocytes with mechanical stretch 48 h; Ad-HSF1+MS: cardiomyocytes infected by adenovirus-expressing HSF1 with mechanical stretch 48 h; Ad-HSF1+MS+PKC inhibitor: cardiomyocytes infected by adenovirus-expressing HSF1and treated with PKC inhibitor with mechanical stretch 48 h). , .

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