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. 2020 Sep 23;42(6):909–920. doi: 10.1038/s41401-020-00526-y

Fig. 1. Transgenic cardiomyocyte-specific overexpression of mitochondrial calpastatin alleviates myocardial injury and dysfunction in hyperglycemic mice.

Fig. 1

a Schematic structure of the transgene. The transgene was released from the vector by digestion with BamH1. hGH: human growth hormone. b A representative Western blot showing transgenic calpastatin (CAST), GAPDH and VDAC1 expression in mitochondria and cytosol in heart tissues from Tg-mtCAST/tTA (TG) mice and their wild-type (WT) littermates. ce Adult Tg-mtCAST/tTA (TG) mice and their wild-type (WT) littermates were injected with streptozotocin (STZ, 50 mg· kg−1· d−1, i.p.) for five consecutive days. Two months after STZ injection, myocardial function was assessed by echocardiography, and necrotic cell death was determined by Evans blue dye (EBD) staining. c Fractional shortening (%). d E/A ratio. e Upper panel: representative microphotographs of Evans blue staining (red) and nuclear staining (blue). Lower panel: quantitation of the percentage of Evans blue-positive area relative to total area (%). The data are presented as the mean ± SD of six different heart tissues from each group. *P < 0.05 vs WT+sham and #P < 0.05 vs WT+STZ.