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Fig. 6 | Cell Communication and Signaling

Fig. 6

From: P38 MAPK activated ADAM17 mediates ACE2 shedding and promotes cardiac remodeling and heart failure after myocardial infarction

Fig. 6

ADAM17 promotes ACE2 shedding in injured cardiomyocyte. A Western blot analysis of ACE2 protein level in H9C2 cardiomyocytes treated with 600 μM hydrogen peroxide for 12 h (n = 3). B RT-qPCR analysis of ACE2 mRNA level. C Western blot analysis of the expression of released ACE2 protein (90 kDa) in the supernatant of cardiomyocytes (n = 5). D After transfection of ADAM17 siRNA to inhibit ADAM17 expression, The mRNA expression level of ACE2 was detected by RT-qPCR (n = 3). E Co-immunoprecipitation of ADAM17 and ACE2 in H9C2 cardiomyocytes. F–H The protein level of ACE2 in cardiomyocytes lysate and supernatant was detected by western blotting (n = 3). I ACE2 activity in cardiomyocytes lysate was detected by the ACE2 activity fluorometric assay (n = 5). J ACE2 activity in cardiomyocyte supernatant was detected by the ACE2 activity fluorometric assay (n = 5). Data shown as mean ± SEM. Derived by two-sample t-test, *P < 0.05; **P < 0.01, ***P < 0.001

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