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. Author manuscript; available in PMC: 2016 Mar 1.
Published in final edited form as: Circ Heart Fail. 2014 Dec 30;8(2):352–361. doi: 10.1161/CIRCHEARTFAILURE.114.001893

Figure 4. Lineage tracing: TNFR1 signaling in development of fibrosis.

Figure 4

Mice (WT with WT-bone marrow [WT/WT], TNFR1-KO with TNFR1-KO-bone marrow [TNFR1-KO/TNFR1-KO], and TNFR1-KO with WT-bone marrow [TNFR1-KO/WT]) were exposed to 7-day Ang-II. A: Perfusion-fixed tissue was stained with picrosirius red for collagen detection; representative images (A1; Suppl.Fig.9) and quantitative analysis (A2) are shown. Chimeric TNFR1-KO/WT mice (n=7) developed interstitial cardiac fibrosis similar to WT/WT mice (n=5) and more than TNFR1-KO/TNFR1-KO mice (n=4). B: Transcriptional activation of selected genes. Chimeric TNFR1-KO/WT mice (n=9) showed increased mRNA levels of collagen-types -I and -III, TNF, IL-1β, and TGF-β1, similar to WT/WT levels (n=6) and higher than TNFR1-KO/TNFR1-KO levels (n=3). C: Perfusion-fixed tissue was stained for TNFR1 and αSMA; representative images are shown (blue = nuclear DAPI; quantification: Suppl.Fig.10). Statistics: (*) indicates a statistically significant difference between TNFR1-KO/TNFR1-KO and TNFR1-KO/WT groups (Kruskal-Wallis, Dunn's). NS: not significant.