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. 2020 Dec 7;28(4):1398–1417. doi: 10.1038/s41418-020-00669-9

Fig. 2. Enhanced coronary angiogenesis, inhibition of ventricular cardiomyocyte apoptosis, and maintenance of sarcomeric structure in the absence of Pkm2.

Fig. 2

A Quantification of capillary density at 4-d post MI (left), as determined in myocardial LV cross-sections employing anti-Von Willebrand factor (Vwf) staining (right; green). Data are mean ± s.e.m. n = 6. *P < 0.01 vs. sham/Veh-control. #P < 0.01 vs. sham/Pkm2KOi. B Quantification of cardiomyocyte apoptosis (left) in LV sections (right) at 2-d post MI. White asterisks, CM. n = 6. Data are mean ± s.e.m. *P < 0.01 vs. Sham/Veh-control. #P < 0.01 vs. sham/Pkm2KOi. C Quantification of cardiac-specific gene expression in LV specimen at 21-d post MI as analyzed by RT-qPCR. Data are means ± s.e.m. n = 4. *P < 0.01 vs. Sham/Veh-control. #P < 0.01 vs. sham/Pkm2KOi. D Immunoblot analysis of cardiac-specific gene expression in LV extracts at 21-d post MI employing antibodies as indicated on the left. Western blots were repeated at least once with similar results employing two independent biological replicates. E Loss of sarcomeric Z-disk structure as indicated by loss of a striated actinin pattern in Veh-control animals at 4-d post MI as assessed using α-actinin antibodies specific to cardiac Z-disks. One representative result of three independent experiments is shown.