Fig. 1: Hsp27 knockdown inhibits glycolysis in hypoxic cardiomyocytes. | Cell Death Discovery

Fig. 1: Hsp27 knockdown inhibits glycolysis in hypoxic cardiomyocytes.

From: Upregulation of Hsp27 via further inhibition of histone H2A ubiquitination confers protection against myocardial ischemia/reperfusion injury by promoting glycolysis and enhancing mitochondrial function

Fig. 1

A Pathway enrichment statistics for the identified mRNA. B Heat map showing upregulated mRNA of the MAPK signaling pathway in the rat heart after 30 min of ischemia. Color-coded representation of gene expression levels: Blue and red represented low and high expression, respectively. Data are representative of three independent experiments. C Immunofluorescence images of Hsp27 (red) staining in cardiomyocytes cultured with or without Hsp27 knockdown after 12 h of hypoxia. D Culture medium acidification following Hsp27 depletion in 12-h hypoxic cardiomyocytes. E Heat map showing glycolytic intermediates 12 h after hypoxia stimulation. Color-coded representation of gene expression levels: Green and red represented low and high expression, respectively. F–G Graphs showing the results of glycolytic stress analyses using a Seahorse XF analyzer to assess the response of cardiomyocytes to oligomycin, glucose, and 2-DG. H Intracellular ATP levels in cardiomyocytes. I–J Detection of cardiomyocyte viability. Data are presented as mean ± SD (n = 6). #P < 0.05 vs. Control group; *P < 0.05 vs. Hypoxia group. Scale bars: (C) 50 μm; (I) 100 μm.

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