Research Paper Volume 11, Issue 24 pp 11955—11974

Figure 4. A lack of platelet β2M increased cardiac fibrosis. (A) Plt-β2M^-/- mice had increased activated fibroblast markers with age. RNA was isolated from single cell cardiac tissue suspensions and qRT-PCR for Acta2, Postn, Fn1, and Col1a2 performed (N=3, mean ± SD, *P<0.05, **P<0.01, one-way ANOVA with Bonferroni correction). (B) Plt-β2M^-/- mice had an age associated increase in cardiac fibrosis. Representative images of Picrosirius staining of hearts from 2.5-mos and 14-mos old WT and Plt-β2M^-/- mice (10x magnification, scale bar=300μm). Images were pooled from 3 WT young and Plt-β2M^-/- young mice, 7 mice of WT old and 10 mice for Plt-β2M^-/- old. Image quantification was performed on ImageJ (mean ± SEM, *P<0.05, unpaired t-test with Welch’s correction). (C) Plt-β2M^-/- mice had an age-related decline in cardiac function. Echocardiography was performed on WT and Plt-β2M^-/- mice (mean ± SEM, *P<0.05 vs young, one-way ANOVA with Bonferroni correction). (D) WT and Plt-β2M^-/- mice had similar heart size. Whole hearts and the right tibia were isolated, heart weight determined and normalized to tibia length (mean ± SEM, one-way ANOVA with Bonferroni correction).