详细记录  
题名:Chronic high glucose-induced INS-1beta cell mitochondrial dysfunction: a comparative mitochondrial proteome with SILAC.
作者:CHEN X; CUI Z; WEI S; HOU J; XIE Z; PENG X; LI J; CAI T; HANG H; YANG F;
来源:Proteomics. 2013 Aug 19. doi: 10.1002/pmic.201200448. [ IF= 4.13 ] ]
URL :10.1002/pmic.201200448
日期:20130902
摘要:As glucose-stimulated insulin secretion (GSIS) of pancreatic beta cell is
triggered and promoted by the metabolic messengers derived from mitochondria,
mitochondria take a central stage in the normal function of beta cells. beta
cells in diabetics were chronically exposed to hyperglycemia stimulation, which
has been reported to exert deleterious effects on beta cell mitochondria.
However, the mechanism of the toxic effects of hyperglycemia on beta cell
mitochondria was not clear. In this study, we characterized the biological
functional changes of rat INS-1beta cells and their mitochondria with chronic
exposure to hyperglycemia and created a research model of chronic
hyperglycemia-induced dysfunctional beta cells with damaged mitochondria. Then,
SILAC-based quantitative proteomic approach was used to compare the mitochondrial
protein expression from high glucose treated INS-1beta cells and control cells.
The expression of some mitochondrial proteins was found with significant changes.
Functional classification revealed most of these proteins were related with
OXPHOS, mitochondrial protein biosynthesis, substances metabolism, transport and
cell death. These results presented some useful information about the effect of
glucotoxicity on the beta cell mitochondria. This article is protected by
copyright. All rights reserved.

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