Essop M F, Chan W A, Hattingh S
Department of Physiological Sciences, Stellenbosch University, Stellenbosch, South Africa.
Cardiovasc J Afr. 2011 Jul-Aug;22(4):175-8. doi: 10.5830/CVJA-2010-058. Epub 2010 Sep 11.
Impaired mitochondrial function may contribute to the onset of contractile dysfunction with insulin resistance/type 2 diabetes. Our aim was therefore to determine alterations in the mitochondrial proteome of a mouse model of obesity/type 2 diabetes.
Mitochondrial proteins were isolated from hearts collected from 18- to 20-week-old female db/db mice and compared to matched controls. We performed two-dimensional polyacrylamide gel electrophoresis to determine differentially expressed proteins. Peptides of interest were further analysed by mass spectrometry and Mascot software was employed to identify protein matches.
Our data showed that ATP synthase D chain, ubiquinol cytochrome-C reductase core protein 1 and electron transfer flavoprotein subunit alpha peptide levels were altered with obesity. Moreover, we found coordinate downregulation of contractile proteins in the obese heart, i.e. α-smooth muscle actin, α-cardiac actin, myosin heavy-chain α and myosin-binding protein C.
We propose that decreased contractile protein levels may contribute to contractile dysfunction of hearts from diabetic mice.
线粒体功能受损可能导致胰岛素抵抗/2型糖尿病患者出现收缩功能障碍。因此，我们的目的是确定肥胖/2型糖尿病小鼠模型线粒体蛋白质组的变化。
从18至20周龄雌性db/db小鼠心脏中分离出线粒体蛋白，并与配对的对照组进行比较。我们进行二维聚丙烯酰胺凝胶电泳以确定差异表达的蛋白质。对感兴趣的肽段进一步进行质谱分析，并使用Mascot软件识别匹配的蛋白质。
我们的数据表明，肥胖会改变ATP合酶D链、泛醇细胞色素C还原酶核心蛋白1和电子传递黄素蛋白亚基α肽的水平。此外，我们发现肥胖心脏中收缩蛋白协同下调，即α-平滑肌肌动蛋白、α-心肌肌动蛋白、肌球蛋白重链α和肌球蛋白结合蛋白C。
我们认为收缩蛋白水平降低可能导致糖尿病小鼠心脏收缩功能障碍。
Zotero 插件