Fig. 4: Targeted analysis of extracellular matrix remodeling response at disease onset in D2-mdx and B10-mdx hearts. | Cell Death & Disease

Fig. 4: Targeted analysis of extracellular matrix remodeling response at disease onset in D2-mdx and B10-mdx hearts.

From: Failure to resolve inflammation contributes to juvenile onset cardiac damage in a mouse model of Duchenne muscular dystrophy

Fig. 4

A qRT-PCR analysis of a distinct cohort of D2-mdx and B10-mdx hearts to assess the expression of extracellular matrix-associated genes involved in matrix organization/re-organization (Fn1, Col1a1, Itgax, Spp1, Mmp12, Timp1) that are identified to be dysregulated by the RNAseq cohort. Relative gene expression values normalized to internal Hprt transcript levels. B-C. Images showing extracellular matrix distribution visualized using wheat germ agglutinin (WGA, pink) within, and surrounding, areas of cardiac damage in juvenile D2-mdx (B), and B10-mdx (C). B’, C’ Zoom of the dotted area from whole cross-sectional images showing immunostaining for COL1A1 within the extracellular matrix shows increased COL1A1 expression in damaged D2-mdx hearts (B’), relative to B10-mdx (C’), indicative of early-onset endomysial fibrosis. Data represent median ± IQR from n = 7−9 hearts per cohort. Statistical analyses performed using non-parametric Mann–Whitney test; **p < 0.01, ***p < 0.001. For age-matched WT controls, refer to Supplementary Fig. 4.

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