Figure 1: miR-182 upregulation in the heart subsequent to PlGF-induced angiogenesis is dependent on NO-induced RGS4 degradation mechanism.
From: miR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart

(a) Increased miR-182 expression in PlGF mice, after 6 weeks of angiogenic stimulation, is concurrent with the development of hypertrophy. miR-182 is not induced in PlGF/RGS4 mice, where hypertrophic response is inhibited. n = 6 (3 wk controls); 6 (3wk PlGF); 6 (3 wk PlGF/RGS4); 6 (6 wk controls); 5 (6 wk PlGF); 6 (6 wk PlGF/RGS4). (b) In situ hybridization of LV myocardium sections with DIG labeled miRCURY LNA mmu-miR-182 detection probe or DIG labeled miR-scramble probe. (c) miR-182 is not upregulated in PlGF-induced eNOS−/− mice, where the hypertrophic response is inhibited. n = 6 (controls); 5 (PlGF); 5 (eNOS−/−); 8 (PlGF/eNOS−/−). *P < 0.05; **P < 0.01.