Fig 1: Deletion of 5-HT2B inhibits the TGF-ß signaling pathway and enhances the inflammatory response. (A) Schematic overview of the AOM/DSS model of acute colitis in mice. (B) Body weight of WT (n = 8) and Htr2b?IEC (n = 8) mice during AOM/DSS treatment. (C) The colon length and colitis severity score of WT and Htr2b?IEC mice (n = 6-8) with acute colitis. (D) H&E staining of colon sections from WT and Htr2b?IEC mice with acute colitis on day 15. (E) Proinflammatory cytokine mRNA levels (n = 3) in whole colonic mucosa specimens from WT and Htr2b?IEC mice. (F) Levels of total protein and phosphorylated JunD, SMAD2, and SMAD3 in the colonic epithelium of WT and Htr2b?IEC mice. (G) SMAD4 protein levels in the colonic epithelium of WT and Htr2b?IEC mice. (H) Levels of total protein and phosphorylated ERK in the colonic epithelium of WT and Htr2b?IEC mice. (I) Levels of total protein and phosphorylated STAT3 in the colonic epithelium of WT and Htr2b?IEC mice. Scale bars, 100 µm. Error bars represent the mean ± SEM. ns: not significant, *P < 0.05, **P < 0.01, ***P < 0.001; Two-way ANOVA (B), unpaired Student's t-test (C) and One-way ANOVA (E).
Fig 2: Potential mechanisms of SUMO1 in different heart cell types after myocardial infarction (MI). In cardiomyocytes, SUMO1 represses Nppa and Nppb transcription and reduces the distribution of Nppa+ Nppb+cardiomyocyte (CM) in injured myocardium in a JunD-dependent manner after MI. In fibroblasts, SUMO1 mediated cardiac repair, promoting the conversion of proliferating fibroblasts to collagen-secreting fibroblasts after myocardial damage. In endothelial cells, SUMO1 inhibited vascular endothelial growth factor A (VEGFA)-mediated angiogenic signaling and inhibited FABP+ endothelial cell (EC) proliferation and revascularization after MI.
Fig 3: Deletion of SUMO1 promoted the proportion of Nppa+Nppb+Ankrd1+ CM subcluster. (A) UMAP visualization of clustering revealed six distinct CM populations. (B) Dot plot showing enriched genes for each CM subclusters. (C) Fraction of each CM subcluster relative to all CMs in each group. (D) Line plot showing changes in the relative fractions of CM3 cluster in each group. (E) Violin plots of natriuretic peptide A (Nppa), natriuretic peptide B (Nppb) and ankyrin repeat domain 1 (Ankrd1) in cardiomyocyte clusters. (F) The atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) mRNA levels in WT and SUMO1-/- mice after Sham and MI (n = 8). (G) Representative images of immunofluorescence of cardiac troponin T (Tnnt2) (green) and Ankrd1 (red) in heart sections from mice after MI. (H) Heatmap of top 40 highly variable transcription factor among the six cardiomyocyte subclusters. The z-scores of TF activities are colour-coded. (I) The heart homogenates were immunoprecipitated with anti-JunD agarose beads and probed with anti-SUMO1 antibody (n = 6). Mean ± standard error of mean (SEM), ***P < 0.001 vs. Sham or MI. UMAP: uniform manifold approximation and projection; CM: cardiomyocyte; MI: myocardial infarction; WT: wild-type; TF: transcription factor.
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