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. 2023 Feb 15;133(4):e156436. doi: 10.1172/JCI156436

Figure 3. Infiltrating myeloid cells are the major source for increased MAPK1 activation in a preclinical model of non-reperfused MI.

Figure 3

Confocal microscopy of whole LV myocardial cryosections obtained from n = 3–5 C57BL/6J mice after 7 days of permanent LAD ligation. (A) Representative images of p-ERK1/2+ cells costained for CD31, CD45, α-SMA, cTNT. Scale bars: 500 μm. (B) Top: Quantification of p-ERK1/2+ intensity in remote, border, and infarction regions at days 1, 3, and 7 after MI. Bottom: Quantification of colocalization analysis of p-ERK1/2 signal intensity with CD31, CD45, α-SMA, and cTNT in border and infarct regions at day 7 after MI using Pearson’s correlation coefficient. RAU, relative arbitrary units. (C) Experimental design: C57BL/6J mice were subjected to permanent LAD ligation versus sham surgery and given trametinib (1 mg/kg/d) or vehicle treatment once daily via oral gavage from day 1 to day 7. (D) High-frequency ultrasound echocardiography obtained in parasternal long axis with measurement of LV ejection fraction (LVEF, %) and LV end-diastolic volume (LVEDV, μL) on day 7 after operation. Ordinary 1-way ANOVA, Šidák’s multiple-comparison test; n = 4–6 animals per group. Data are shown as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.