Proteomics analysis on stressed myocardium injury-related proteins / 中国应用生理学杂志

<p><b>AIM</b>To probe the related proteins to stress-induced myocardium injury.</p><p><b>METHODS</b>After establishment of a myocardium injury model induced by restraint stress in rats, myocardium proteins of restraint stress-treated and untreated rats were extracted, and the two-dimensional polyacrylamide gel electrophoresis (2-DE) maps of the extracted proteins were established by using the immobilized pH gradient (IPG) and SDS-PAGE two-dimensional electrophoresis respectively. The alterative protein spots were analyzed by Image Master 3.01 software and identified with assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF-MS) and database searching.</p><p><b>RESULTS</b>Proteomics analysis showed that there were 10 proteins were significantly influenced by restraint stress in rat myocardium. After stress, proteins, including cardiac myosin heavy chain, dihydrolipoamide succinyltransferase component of 2-oxoglutarate dehydrogenase complex, similar to dihydrolipoamide S-succinyltransferase, mitochondrial aldehyde dehydrogenase, H (+)-transporting ATP synthase, albumin, myosin heavy chain and apolipoprotein A-I precursor showed increased expression. Mitochondrial aconitase and uncoupling protein UCP-3 showed decreased expression.</p><p><b>CONCLUSION</b>These differential expressive proteins might be involved in stress-induced injury to myocardium.</p>

Effect of homocysteine on injury of cardiomyocytes and its signal transduction mechanism / 中国应用生理学杂志

<p><b>AIM</b>To observe the injured effect of homocysteine (HCY) on cardiomyocytes and investigate its signal transduction mechanism as well as the key regulatory link.</p><p><b>METHODS</b>Cardiomyocytes were isolated from neonatal Wistar rats. After incubation with HCY, the survival rate of cardiomyocytes was determined by trypan blue stained assay, while the apoptosis rate was measured by TUNEL and FCM. Western blot and EMSA were used to tested ERK2 protein phosphorylation and NF-kappaB active expression in cardiomyocytes, respectively.</p><p><b>RESULTS</b>The survival rate of cardiomyocytes treated with HCY was reduced significantly in dose- and time- dependent manner. It was found that 10(-3) mol/L HCY could increase the apoptosis rate of cardiomyocytes to the peak (7.65%) at 4 h stress. Several HCY levels revealed the strong inhibitory effect on ERK2 protein phosphorylation, especially, 10(-3) mol/L HCY decreased the level of active ERK2 expression to 3.04% of control at 4 h (P < 0.01). NF-kappaB activation was also inhibited significantly by several HCY level for different time in cardiomyocytes.</p><p><b>CONCLUSION</b>HCY plays an important role in injury of cardiomyocytes and apoptosis is a form of HCY-induced injury to cardiomyocytes. HCY can block ERK2 protein phosphorylation and NF-kappaB activation, which contribute to the injury of cardiomyocytes.</p>