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. 2018 Oct 23;8:15633. doi: 10.1038/s41598-018-34112-4

Figure 6.

Figure 6

Serca2a knockdown increases resistin and NFATc expression in adult mice. Heart tissues of Serca2a knockout or wildtype mice were analyzed for Serca2a, resistin and nuclear NFATc expressions by western blotting (A) with densitometry quantification shown (B). §§p < 0.01 vs wildtype. The expression of nuclear NFATc mRNA was analyzed in hearts from diabetic ob/ob and Serca2a-deficient mice (Serca2a−/−) (C). Ob/ob diabetic mice were infected with AAV9-Serca2a or AAV9-empty vectors and protein expression of resistin, nuclear NFATc, and phosphorylation of AMPKα were analyzed by western blotting (D) with densitometry quantifications shown (E,F). The expression of nuclear NFATc mRNA was analyzed in AAV9-Serca2a or AAV9-empty vector infected ob/ob mice hearts (G). 18S rRNA was used as an internal control for q-PCR. The phosphorylation of AMPK status is presented as phospho-AMPK/AMPK ratio. H3 and β-actin was used as corresponding internal controls for western blotting. The data are mean ± SEM of three experiments from 5–6 animals. $$p < 0.01 lean vs Ob/ob; $$$p < 0.001 lean vs Serca2a−/− (C) *p < 0.05 lean vs ob-Empt, and ob-Empt vs AAV9-Serca2a (E and F); ***p < 0.001 ob/ob-Empt vs AAV9-Serca2a (G) ###p < 0.001 lean vs ob/ob-Empt (G).