Hyperglycemia disrupts mitochondrial network formation and cardiac myofibrilogenesis, while cardiogenic TGF-β augments adenylate kinase expression.

Abstract

<p>A – Excess glucose (50 mM) stunted beating activity through day 12. <b>B</b> and <b>C</b> - Beating areas visualized using JC-1 (green) and membrane potential marker RH 237 (red) in control (<b>B</b>) and high glucose grown embryoid bodies (<b>C</b>). <b>D</b> and <b>E</b> – Mitochondrial distribution in cardiomyocytes from control (<b>D</b>) and glucose-treated embryoid bodies (<b>E</b>) visualized using MitoTracker Red. F and G – Myofibrillar formation and organization in control CM (<b>F</b>) versus glucose treated CM (<b>G</b>) assessed by cardiac specific MLC2v-GFP expression. <b>H</b> – Differential AK1 and AK2 immunofluorescent signals in control ES cells (upper) and those treated with TGF-β (lower). <b>I</b> – TGF-β treatment increased AK1 protein levels quantified by Western blot (left) and adenylate kinase activity (right). Scale bars in B, C and H are 20 µm, in D, E, F and G - 10 µm. Representative images and data of n = 3–5.</p