Fig. 3

Selective depletion of αv integrins on PDGFRβ⁺ cells is protective in cardiac fibrosis. a Immunofluorescence micrographs of heart muscle from mTmG;Pdgfrb-Cre mice co-stained with anti-PDGFRβ (scale bar 5 μm), anti-CD31 (scale bar 5 μm) and anti-myosin antibodies (scale bar 30 μm). b, c Quantification of GFP reporting and PDGFRβ antibody staining colocalisation in cardiac muscle (n = 6). d Overview of the cardiac fibrosis model. Mice were treated with 200 ng kg⁻¹ min⁻¹ AngII or vehicle control for 14 days prior to harvest and analysis of tissues. e Immunofluorescence micrographs of heart sections from control or AngII-treated mTmG;Pdgfrb-Cre mice. Scale bars 30 μm. f Percentage field coverage of PDGFRβ⁺ cells at day 14 in vehicle control or AngII-treated mTmG;Pdgfrb-Cre mice (n = 3). g Quantitation of GFP⁺ nuclei at day 14 in vehicle control or AngII-treated mTmG;Pdgfrb-Cre mice (n = 4) h qPCR of Col1a1 in cardiac PDGFRβ⁺ cells sorted from AngII injured and control hearts (n = 5) i qPCR of Col1a1 in cardiac PDGFRβ⁺ cells activated in culture for 5 days (n = 3). j Blood pressure response of control and Itgav ^flox/flox;Pdgfrb-Cre (αv Cre) mice to AngII treatment or vehicle (n = 6). k Picrosirius red staining of cardiac tissue 14 days after commencement of AngII treatment in control and Itgav ^flox/flox;Pdgfrb-Cre mice. Scale bars 1 mm in whole heart sections, 70 μm for magnified fields. l Digital image analysis of collagen staining (n = 6 mice per group). Data are expressed as mean ± SEM. *P < 0.05, **P < 0.01 (Student’s t-test)