Fig. 4: TLR9 deficiency aggravated cardiomyocyte and fibroblast apoptosis post-MI. | Cell Death & Disease

Fig. 4: TLR9 deficiency aggravated cardiomyocyte and fibroblast apoptosis post-MI.

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

Fig. 4

a Representative TUNEL and α-actinin staining of cardiac myocytes in heart sections from WT and TLR9KO mice at day 3 after MI (n = 6; bar = 50 μm). Green color was TUNEL staining representing apoptotic cells; red color was the α-actinin staining representing cardiac myocytes; blue color was the cell nucleus stained by DAPI. b Representative TUNEL and vimentin staining in heart sections from WT and TLR9KO mice at day 3 after MI (n = 6; bar = 50 μm). Green color was TUNEL staining representing apoptotic cells; red color was the vimentin staining representing fibroblasts; blue color was the cell nucleus stained by DAPI. c Cleaved caspase-3 expression in the heart sections of the WT and TLR9KO mice post-MI after 7 days determined by immunohistochemistry (n = 3; bar = 50 μm). d–f Western blot was used to detect the protein levels of Bax, Bcl-2, and Bcl-xl in mice for each group, then the apoptotic index, Bcl-2/Bax, and Bcl-xl/Bax of each group were calculated and analyzed. NS indicates not significant; *P < 0.05 vs. WT sham group; §P < 0.05 vs. WT MI group; &P < 0.05 vs. WT MI mice in infarct area; #P < 0.05 vs. WT MI mice in border area

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