Extended Data Fig. 3: Cardiovascular disease-induced structural changes in bone marrow vasculature.
From: Bone marrow endothelial dysfunction promotes myeloid cell expansion in cardiovascular disease

a, b, Immunohistochemical staining for collagen III (a) and quantification of collagen I (Coll-I) and collagen III (Coll-III) (b) in hypertensive Ang-II-treated mice (Coll-I: saline n=15, Ang-II n=18; Coll-III: saline n=15, Ang-II n=16; two-tailed Welch’s t-test). c, Representative confocal immunofluorescence microcopy (tile scans) displaying the distribution of CD31+Sca-1+ blood vessels across the distal femoral bone marrow of naive controls, mice with Angiotensin II induced arterial hypertension (HTN), atherosclerotic Apoe−/− mice on Western diet (Athero), and mice 6 days after myocardial infarction (MI).d, Quantification of blood vessel area (n=6 fields of view from n=6 controls and n=4 HTN/Athero/MI mice, one-way ANOVA with Dunnett’s T3 post-test).e, CD31 immunohistochemistry obtained in M. quadriceps femoris from naive controls, mice with Angiotensin II-induced arterial hypertension (Ang-II) and mice on day 6 after MI. Arrowheads indicate CD31+ capillaries. g, Flow plots and quantification of endothelial cells in the M. quadriceps femoris of controls and mice 6 days post myocardial infarction (n=8 mice per group, two-tailed Welch’s t-test). h, Quantification of endothelial cells in the spleen of WT and Apoe−/− mice with atherosclerosis by flow cytometry (n=10 WT mice, n=8 Apoe−/−, two-tailed Welch’s t-test). Data are displayed as mean±SEM.