Fig. 6: Effect of rhHMGB1 on WT and TLR9KO mice post-MI survival, ventricular rupture, myocardial fibrosis, and cardiac function. | Cell Death & Disease

Fig. 6: Effect of rhHMGB1 on WT and TLR9KO mice post-MI survival, ventricular rupture, myocardial fibrosis, and cardiac function.

From: TLR9 is essential for HMGB1-mediated post-myocardial infarction tissue repair through affecting apoptosis, cardiac healing, and angiogenesis

Fig. 6

a Kaplan–Meier survival analysis post-MI in WT (n = 23), TLR9KO (n = 23), WT-rhHMGB1 (n = 24), and TLR9KO-rhHMGB1 (n = 21)mice. b Incidence of cardiac rupture in WT, TLR9KO, WT-rhHMGB1, and TLR9KO-rhHMGB1 mice at day 28 post-MI. Data were analyzed by chi-squared test. c TTC staining (left) in WT, TLR9KO, WT-rhHMGB1, and TLR9KO-rhHMGB1 mice at day 3 after MI and quantitative analysis of infarct size (middle) and wall thickness of the infarct regions (right) (n = 5–6). d Representative PSR staining sections of in WT, TLR9KO, WT-rhHMGB1, and TLR9KO-rhHMGB1 mice heart at day 14 after MI (left; bar = 50 μm). Quantification of fibrotic areas in infarct and border areas (middle, n = 6). at day 14 post-MI in in WT, TLR9KO, WT-rhHMGB1, and TLR9KO-rhHMGB1 mice (right, n = 6). e Evaluation of cardiac function in WT, TLR9KO, WT-rhHMGB1, and TLR9KO-rhHMGB1 mice. Quantitative analysis of left ventricular end-diastolic diameter (LVEDD), fractional shortening (FS), ejection fraction (EF) at day 28 after the MI or sham operation (n = 6). NS indicates not significant; *P < 0.05; §P < 0.05 vs. PBS-treated WT MI group; #P < 0.05 vs. rhHMGB1-treated WT MI group

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