AIM:To identify the changes of mitochondrial protein expression in diabetic renal parenchyma and to characterize their molecular functions and biological processes in diabetes. METHODS:Mitochondrial proteins extracted from renal parenchyma mitochondria of streptozotocin-induced diabetic rats and normal rats were separated by two-dimensional polyacrylamide gel electrophoresis and identified by matrix-assisted laser desorption/ionization tandem time-of-flight mass spectrometry. RESULTS:Eleven proteins from 533 visualized protein spots displayed significant different expressions in mitochondria of diabetic kidneys compared with those in normal ones. Among these altered proteins, two proteins with the most obvious changes in protein expression were identified as alpha-2u globulin (mature protein, named A2) and its proteolytically modified form (named A2-fragment) respectively. These proteins were found in mitochondria of male rat renal parenchyma and were proved to be down-regulated in diabetic rats simultaneously. CONCLUSION:Our results suggest that down-regulation of alpha-2u globulin may be associated with an abnormal β-oxidation of long-chain fatty acids during diabetes. The decreased expression of A2-fragment in renal mitochondria of diabetic nephropathy may reduce fatty acid β-oxidation, which leads to a diminished energy supply from mitochondria to kidney tissue and the deposition of a large number of fatty acids in the kidney, ultimately causing and aggravating kidney damage. In conclusion, these findings may be helpful for understanding the molecular mechanism of diabetic nephropathy.

译文

目的:确定糖尿病肾实质中线粒体蛋白表达的变化,并对其在糖尿病中的分子功能和生物学过程进行表征。
方法:采用二维聚丙烯酰胺凝胶电泳分离从链脲佐菌素诱发的糖尿病大鼠和正常大鼠的肾实质线粒体中提取的线粒体蛋白,并通过基质辅助激光解吸/电离串联时间质谱法进行鉴定。
结果:533个可视化蛋白斑点中的11种蛋白在糖尿病肾线粒体中的表达与正常肾脏相比明显不同。在这些改变的蛋白质中,两个蛋白质表达变化最明显的蛋白质分别被鉴定为alpha-2u球蛋白(成熟蛋白质,称为A2)及其蛋白水解修饰形式(称为A2片段)。这些蛋白在雄性大鼠肾实质的线粒体中发现,并被证明在糖尿病大鼠中同时被下调。
结论:我们的结果表明,糖尿病患者中α-2u球蛋白的下调可能与长链脂肪酸的β-氧化异常有关。糖尿病肾病肾脏线粒体中A2片段的表达降低可能会降低脂肪酸β氧化,从而导致线粒体向肾脏组织的能量供应减少以及大量脂肪酸在肾脏中的沉积,最终导致和加重肾脏损害。总之,这些发现可能有助于理解糖尿病性肾病的分子机制。

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