Skip to main content
. Author manuscript; available in PMC: 2024 Mar 13.
Published in final edited form as: J Cell Physiol. 2021 Apr 30;236(11):7578–7590. doi: 10.1002/jcp.30401

FIGURE 3.

FIGURE 3

The ablation of TIGAR increases capillary density and coronary flow reserve (CFR) in normal hearts. (a) Representative immunoblots and quantitative analysis of TIGAR, Angiopoietin-1 (Ang-1), VEGF, GAPDH, and β-tubulin in the indicated mouse hearts (n = 3). *p < .05, ***p < .001. (b) The representative images of Isolectin B4 (IB4, green; DAPI stains the nuclei, blue)-stained frozen heart sections and quantification of the number of capillaries/100 nuclei in the indicated groups (n = 3). *p < .05. Bar = 50 μm. (c) The representative images of α-smooth muscle actin (α-SMA, red; DAPI stains the nuclei, blue)-stained frozen heart sections and quantification of the number of arterioles/field in the indicated groups (n = 3). (d) The representative pulsed-wave Doppler images of the proximal left coronary arteries of WT and TIGAR KO mice at 16–20 weeks of age. CFR was calculated as the ratio of hyperemic peak diastolic flow velocity (2.5% isoflurane) to baseline peak diastolic flow velocity (1% isoflurane) in the indicated groups (n = 17). *p < .05. DAPI, 4′,6-diamidino-2-phenylindole; KO, knockout; TIGAR, TP53-induced glycolysis and apoptosis regulator; WT, wild type