MAFbx and MuRF1 mRNA expression and its relationship with muscular contractility following free muscle transfer / 中华整形外科杂志

<p><b>OBJECTIVE</b>To study muscle atrophy F-box (MAFbx) and muscle ring finger 1 (MuRF1) mRNA expression and its relationship with muscular contraction following free muscle transfer.</p><p><b>METHODS</b>The gracilis muscle was orthotopic transferred in adult rat to establish the animal model. The muscle at the unoperated side was used as control. The expression of MAFbx and MuRF1 mRNA, the muscle contraction and muscle function were measured by real-time PCR and multiple function physiological device. The relationship among the expression of MAFbx and MuRF1 mRNA, the muscle contraction and muscle function was analyzed.</p><p><b>RESULTS</b>After muscle free transfer, muscle wet weight reservation, the maximum contraction and tetanus strength reduce first and increased later, but still lower than those at control side. The expression of MAFbx and MuRF1 mRNA reached peak level 3 - 4 weeks after muscle transfer which was 7.1 and 4.1 times as that at control side. It decreased later, but still higher than that at control side, showing a significant difference between them (P< 0. 05).</p><p><b>CONCLUSIONS</b>Persistent over-expression of MAFbx and MuRF1 mRNA after muscle transfer has a close relationship with muscle atrophy and muscle dysfunction. MAFbx and MuRF1 can be used as markers for early muscle atrophy, and also as potential target for drug treatment of muscle atrophy.</p>

Involvement of endothelin-1 in hypoxia-induced cardiomyocyte apoptosis / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effect of endogenous endothelin-1 (ET-1) on cardiomyocyte apoptosis induced by hypoxia and its possible mechanism.</p><p><b>METHODS</b>Cultured neonatal rat cardiomyocytes were divided into control group and ET receptor antagonist group. Control group was given DMEM only and ET receptor antagonist group was treated with ET receptor subtype A (ET(A)) receptor antagonist BQ610 and BQ123 or ET(B) receptor antagonist BQ788 and subjected to hypoxia for 24 h. The presence of apoptosis in cardiomyocytes was evaluated by TUNEL analysis and flow cytometry (FCM).</p><p><b>RESULTS</b>TUNEL analysis showed that the percentage of positive apoptotic cells in BQ610 5 micromol/L group was 13.2% +/- 3.7%, significantly lower than that in hypoxia group (24.2% +/- 2.2%, P < 0.01). FCM showed that BQ123 (0.04, 0.2 and 1.0 micromol/L) inhibited hypoxia-induced cardiomyocyte apoptosis and increased cardiomyocyte survival rate in a dose-dependent manner, while BQ788 did not show such effects.</p><p><b>CONCLUSION</b>These findings suggest that endogenous ET-1 aggravates hypoxia-induced cardiomyocyte apoptosis and this effect is mediated through ET(A) receptor-dependent pathways.</p>

Endothelin signaling in cardiac myocyte / 中国医学科学院学报

Endothelin can affect the contractile properties of cardiacmyocyte, stimulate myocyte growth and myofibrillogenesis, and increase resistance to apoptosis by intracellular signaling pathways. This article briefly reviews the regulative effects of these signaling pathways including protein kinase C, mitogen activated protein kinase, and phosphoinositide 3'-OH kinase/protein kinase B.