Proteomic analysis of mitochondrial proteins in a mouse model of type 2 diabetes
dc.contributor.author | Essop M.F. | |
dc.contributor.author | Chan W.A. | |
dc.contributor.author | Hattingh S. | |
dc.date.accessioned | 2011-10-13T16:59:17Z | |
dc.date.available | 2011-10-13T16:59:17Z | |
dc.date.issued | 2011 | |
dc.description.abstract | Objective: 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. Methods: 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. Results: 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. Conclusion: We propose that decreased contractile protein levels may contribute to contractile dysfunction of hearts from diabetic mice. | |
dc.description.version | Article | |
dc.identifier.citation | Cardiovascular Journal of Africa | |
dc.identifier.citation | 22 | |
dc.identifier.citation | 4 | |
dc.identifier.citation | http://www.scopus.com/inward/record.url?eid=2-s2.0-80052223023&partnerID=40&md5=3a0f99a2f20486a8adbdadcf50f0b322 | |
dc.identifier.issn | 19951892 | |
dc.identifier.other | 10.5830/CVJA-2010-058 | |
dc.identifier.uri | http://hdl.handle.net/10019.1/17054 | |
dc.title | Proteomic analysis of mitochondrial proteins in a mouse model of type 2 diabetes | |
dc.type | Article |