Fig. 5: T8Ab treatment promotes a cardioprotective gene signature in hypertension.
From: ANTXR1 blockade enhances cardiac function in preclinical models of heart failure
a, UMAPs display cardiac cell subpopulations for each treatment group. b, Trajectory analysis of the CF subclusters. c, Violin plot showing the relative Antxr1 and Postn expression in each annotated cell type. d, Bar graph indicates % increase in Antxr1-positive CF4,6 cells versus all the cells after 28 days of ATII/PE. n = 3 per group, and each individual sample was derived by pooling together two hearts to minimize variability. Data represent mean ± s.e.m. e, Co-IF staining for ANTXR1 (green) and THBS4 (red) in the LV 28 days post-ATII/PE. Image is representative of at least three hearts. Scale bar, 200 µm. f, GO analysis comparing enriched pathways in CF1–3 versus CF4,6 post-ATII/PE exposure. g, Volcano plot showing gene expression changes in response to T8Ab treatment in the sham control (top) and ATII/PE treated (bottom) groups. h, Co-IF staining for CHP (red) and WGA (magenta) in LV after 28 days of ATII/PE. Image is representative of at least three hearts. Scale bar, 50 µm. i, Quantification of CHP staining. Data represent mean ± s.e.m. from three independent biological samples, each depicted with a distinct color/shape. For each sample, multiple fields were imaged (small symbols), and the larger symbol corresponds to the average of that sample. j, Violin plot showing Cthrc1, Comp and Acta2 expression. k, qRT–PCR validation of Cthrc1, Comp and Acta2 mRNA expression. n = 3 per group, and each individual sample was derived by pooling together two hearts to minimize variability. P values were assessed using an unpaired, two-tailed t-test (d), one-way ANOVA with Tukey’s multiple-comparisons test (i,k) or two-tailed Wilcoxon test (j). *P < 0.05, ***P < 0.001.
