Extended Data Fig. 3: PdgfrbSMC−Δ/Δ did not result in differences in BCA lesion size or remodeling indices after 18 weeks of WD and ACTA2+ cells co-localize with LGALS3 or CD31 in lesions lacking SMC investment. | Nature Metabolism

Extended Data Fig. 3: PdgfrbSMC−Δ/Δ did not result in differences in BCA lesion size or remodeling indices after 18 weeks of WD and ACTA2+ cells co-localize with LGALS3 or CD31 in lesions lacking SMC investment.

From: Multiple cell types contribute to the atherosclerotic lesion fibrous cap by PDGFRβ and bioenergetic mechanisms

Extended Data Fig. 3: PdgfrbSMC−Δ/Δ did not result in differences in BCA lesion size or remodeling indices after 18 weeks of WD and ACTA2+ cells co-localize with LGALS3 or CD31 in lesions lacking SMC investment.

a, MOVAT representation of PdgfrbSMC-WT/WT and PdgfrbSMC-Δ/Δ mice after 18 weeks of WD. b, Lesion, (c) External elastic lamina (EEL), d, or lumen area were not significantly changed at three locations. e, Necrotic core area was also unchanged. ACTA2 staining co-localizes with LGALS3 (f) or CD31 (g) in the fibrous cap of PdgfrbSMC-Δ/Δ mice. In PdgfrbSMC-WT/WT mice, ACTA2+ eYFP+ cells co-stain with LGALS3 (white) or CD31 (yellow). Scale bar: 100 μm (a) and 20 μm (f, g). X-axis values represent distance past the aortic arch. Graphs were analyzed using two-way ANOVA with Sidak correction and multiple comparisons, biologically independent animals are indicated as individual dots in (b,c,d,e), error bars represent mean ± SEM.

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