Fig 1: MC5R signaling in cardiac hypertrophy induced by high glucose. H9c2 hypertrophy induced by hyperglycemia is characterized by increased miR-133a levels, leading to PI3K inactivation and GLUT1/GLUT4 elevation. Here, we show for the first time an up-regulation of MC5R, involved in glucose-uptake, as a defensive and anti-hypertrophic response to the high-glucose induced damage. MC5R agonism reduced H9c2 hypertrophic markers by decreasing miR-133a levels, consequently restoring PI3K activity and GLUT1/GLUT4 ratio.
Fig 2: Plasma membrane GLUT1 and GLUT4 levels. In line with previous evidences, H9c2 cells exposed to high glucose (33 mM D-glucose) exhibited lower GLUT4 levels and increased GLUT1 levels in plasma membrane, resulting in a higher GLUT1/GLUT4 levels compared to cells exposed to normal glucose (5.5 mM D-glucose). a-MSH (90 pM) and PG-901 (10-10 M) significantly restored GLUT1/GLUT4 ratio, by increasing GLUT4 and consequently decreasing GLUT1 plasma membrane levels. PG-20N MC5R antagonist (130 nM) did not lead to any modification of the high GLUT1/GLUT4 ratio induced by high glucose. Values are expressed as mean ± S.E.M. of n = 9 values, obtained from the triplicates of three independent experiments. NG, normal glucose; Ang II, angiotensin II; HG, high glucose; *P < 0,01 vs. NG; °P < 0,01 vs. HG.
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