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Fig. 4 | Clinical Epigenetics

Fig. 4

From: Multi-omics integration identifies key upstream regulators of pathomechanisms in hypertrophic cardiomyopathy due to truncating MYBPC3 mutations

Fig. 4

Changes of ATP2A/SERCA2a and HSPA2 at the mRNA and protein levels in HCM versus control hearts. a A plot of the joint component loadings of RNA-seq data showed ATP2A2 and HSPA2 were two major players in discriminating HCM hearts from controls. The dashed lines on both positive and negative sides indicate the cutoff threshold, with genes with a large contribution to the joint component falling outside of the dash lines. b ATP2A2 mRNA and protein levels in HCM and control samples at the mRNA and protein levels. c HSPA2 mRNA and protein levels expression in HCM and control samples. **: P < 0.01, ***: P < 0.001, ****: P < 0.0001. d Representative immunohistochemistry staining showing higher HSPA2 staining intensity in HCM heart as compared to control. Scale bar = 400 µm (control sample) and 800 µm (HCM sample). e Representative immunofluorescence staining showing HSPA2 aggregates in an HCM heart (indicated by the arrow), whereas the control shows diffuse staining of the cytoplasm without aggregates. WGA-AF488 appears in gray to visualize the cell membrane, and DAPI appears in blue to visualize the nuclei. Scale bar = 16 µm

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