Cardiomyocyte GATA4 functions as a stress-responsive regulator of angiogenesis in the murine heart
J. Clin. Invest. Joerg Heineke, et al. 117:3198 doi:10.1172/JCI32573 [Go to this article.]

Figure 5
Assessment of the role of hypoxia and vascular rarefaction in promoting heart failure in heart-specific Gata4-deleted mice. (A) EF5 staining for the detection of ischemia from myocardial sections of WT mice and Gata4^β-Cre mice 2 weeks after TAC or without surgery as a control. Stronger intensity of red staining indicates ischemia. Mice with myocardial infarction were used as positive controls, and negative controls consisted of mice without EF5 injection. (B) Western blot analysis of myocardial HIF-1α and LDH expression in WT and Gata4^β-Cre mice without surgery and 2 weeks after TAC. (C) Immunohistochemistry for β-gal protein expression (green) in cryopreserved histological sections from hearts previously treated with Ad–β-gal. (D) Capillary density measurements in control (Gata4^fl/fl and β-Cre) and Gata4^β-Cre mice 7 days after TAC stimulation and heart-specific transduction with the indicated recombinant adenoviruses. *P < 0.01 versus Ad–β-gal control; ^#P < 0.01 versus β-gal treated Gata4^β-Cre mice. (E) Fractional shortening measured by echocardiography 1 week after TAC stimulation and transduction with the indicated viruses in control and Gata4^β-Cre mice. *P < 0.01 versus Ad–β-gal control; ^#P < 0.01 versus Ad–β-gal Gata4^β-Cre. Original magnification, ×100 (A); ×200 (C).