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. 2020 Mar 3;30(9):3149–3163.e6. doi: 10.1016/j.celrep.2020.02.008

Figure 4.

Figure 4

An Epicardial-Derived Injury Response (IR) Fibroblast Population in the Early Phase of Repair Post-MI

(A) Heatmap of the average expression of the top 20 signature IR cluster genes across all fibroblast sub-clusters.

(B) Top cytokines and chemokines produced by the IR cluster.

(C) Top IR cluster canonical pathways identified using Ingenuity Pathway Analysis (IPA).

(D) Confocal imaging of MT1-2 staining in IR fibroblasts at d1 and d3 post-MI using Wt1cre;ZsGreenf/+ and Col1a1eGFP reporter mice.

(E) Scatterplot showing the percentage of MT1-2+ cells co-labeled with the reporter Col1a1eGFP or CD45 (gray). A total of 5–10 frames were counted per each time point, 2–3 mice per time point. Data are represented as means ± SEMs. LV (green dot) is the left ventricle injury site; RV/Distal (red triangle), right ventricle, area distal from the injury site.

(F) SPRING visualization of the IR sub-cluster showing time course evolution of cluster identity (blue arrow) from fibroblast (Fb) to myofibroblast (Myofb). Plots on right panels show marker genes that distinguish early (Fb) from late (Myofb) IR cells. Scale bars, 50 μm.

See also Figure S4 and Tables S3 and S4.