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. 2023 Jan 30;6(4):e202201690. doi: 10.26508/lsa.202201690

Figure 2. Markers of pathological hypertrophy are not up-regulated in MHC-Plin5 cardiomyocytes.

Figure 2.

(A) Representative heart cryosections of 22-wk-old WT and MHC-Plin5 mice stained with fluorescent WGA (red) and CD31 (green). Scale bar, 50 µm. (B) Left, quantification of (A): cardiomyocyte cross-sectional area (CM CSA) (nmice = 7 [WT], 7 [MHC-Plin5]). Right, distribution of CM CSA in all measured cardiomyocytes (calculated from nmice = 7 [WT], 7 [MHC-Plin5]; ncell = 1,400 [WT], 1,394 [MHC-Plin5]). (C) Quantification of (A): vessel density within cardiac tissues (nmice = 7 [WT], 7 [MHC-Plin5]). (D) mRNA expression of the indicated genes in isolated primary cardiomyocytes from 27-wk-old WT and MHC-Plin5 mice (nmice = 9 [WT], 7 [MHC-Plin5] from ≥2 independent isolations). (E) Representative heart cryosections of 27-wk-old WT and MHC-Plin5 mice stained with picrosirius red. Scale bar, 500 µm. (F) Quantification of (E): % fibrosis, percentage area stained with picrosirius red quantified as a percentage of the total area of the heart cryosection (nmice = 10 [WT], 8 [MHC-Plin5]). (G) mRNA expression of the indicated genes in heart from 27-wk-old WT and MHC-Plin5 mice (nmice = 9–10 [WT], 8–9 [MHC-Plin5]). Values are the mean ± SEM; P-values are calculated by a t test.