Mitochondrial proteome analysis reveals altered expression of voltage dependent anion channels in pancreatic beta-cells exposed to high glucose
Ahmed Khandker, Meftun LU ; Jabar Muhammed, Sarheed LU ; Kessler, Benedikt and Salehi, S Albert LU
(2010)
In Islets
2(5).
p.283-292
- Abstract
- Chronic hyperglycemia leads to deterioration of insulin release from pancreatic beta-cells as well as insulin action on peripheral tissues. However, the mechanism underlying beta-cell dysfunction resulting from glucose toxicity has not been fully elucidated. The aim of the present study was to define a set of alterations in mitochondrial protein profiles of pancreatic beta-cell line in response to glucotoxic condition using 2-DE and tandem mass spectrometry. INS1E cells were incubated in the presence of 5.5 and 20 mM glucose for 72 hrs and mitochondria were isolated. Approximately 75 protein spots displayed significant changes (p < 0.05) in relative abundance in the presence of 20 mM glucose compared to controls. Mitochondrial proteins... (More)
- Chronic hyperglycemia leads to deterioration of insulin release from pancreatic beta-cells as well as insulin action on peripheral tissues. However, the mechanism underlying beta-cell dysfunction resulting from glucose toxicity has not been fully elucidated. The aim of the present study was to define a set of alterations in mitochondrial protein profiles of pancreatic beta-cell line in response to glucotoxic condition using 2-DE and tandem mass spectrometry. INS1E cells were incubated in the presence of 5.5 and 20 mM glucose for 72 hrs and mitochondria were isolated. Approximately 75 protein spots displayed significant changes (p < 0.05) in relative abundance in the presence of 20 mM glucose compared to controls. Mitochondrial proteins downregulated under glucotoxic conditions includes ATP synthase a chain and delta chain, malate dehydrogenase, aconitase, trifunctional enzyme beta subunit, NADH-cytochrome b5 reductase and voltage-dependent anion-selective channel protein (VDAC) 2. VDAC 1, 75 kDa glucose-regulated protein, heat shock protein (HSP) 60 and HSP10 were found to be upregulated. The orchestrated changes in expression of VDACs and multiple other proteins involved in nutrient metabolism, ATP synthesis, cellular defense, glycoprotein folding and mitochondrial DNA stability may explain cellular dysfunction in glucotoxicity resulting in altered insulin secretion. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1963969
- author
- Ahmed Khandker, Meftun
LU
; Jabar Muhammed, Sarheed
LU
; Kessler, Benedikt
and Salehi, S Albert
LU
- organization
- publishing date
- 2010
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- proteomics, two-dimensional gel electrophoresis, voltage-dependent, anion-selective channel proteins, mitochondria, insulin secretion, mass, spectrometry
- in
- Islets
- volume
- 2
- issue
- 5
- pages
- 283 - 292
- publisher
- Landes Bioscience
- external identifiers
-
- wos:000289688900004
- ISSN
- 1938-2022
- DOI
- 10.4161/isl.2.5.12639
- language
- English
- LU publication?
- yes
- id
- 23e99724-8fe6-4722-acbe-90128aa66b8d (old id 1963969)
- date added to LUP
- 2016-04-01 10:50:01
- date last changed
- 2019-05-28 02:19:19
@article{23e99724-8fe6-4722-acbe-90128aa66b8d,
abstract = {{Chronic hyperglycemia leads to deterioration of insulin release from pancreatic beta-cells as well as insulin action on peripheral tissues. However, the mechanism underlying beta-cell dysfunction resulting from glucose toxicity has not been fully elucidated. The aim of the present study was to define a set of alterations in mitochondrial protein profiles of pancreatic beta-cell line in response to glucotoxic condition using 2-DE and tandem mass spectrometry. INS1E cells were incubated in the presence of 5.5 and 20 mM glucose for 72 hrs and mitochondria were isolated. Approximately 75 protein spots displayed significant changes (p < 0.05) in relative abundance in the presence of 20 mM glucose compared to controls. Mitochondrial proteins downregulated under glucotoxic conditions includes ATP synthase a chain and delta chain, malate dehydrogenase, aconitase, trifunctional enzyme beta subunit, NADH-cytochrome b5 reductase and voltage-dependent anion-selective channel protein (VDAC) 2. VDAC 1, 75 kDa glucose-regulated protein, heat shock protein (HSP) 60 and HSP10 were found to be upregulated. The orchestrated changes in expression of VDACs and multiple other proteins involved in nutrient metabolism, ATP synthesis, cellular defense, glycoprotein folding and mitochondrial DNA stability may explain cellular dysfunction in glucotoxicity resulting in altered insulin secretion.}},
author = {{Ahmed Khandker, Meftun and Jabar Muhammed, Sarheed and Kessler, Benedikt and Salehi, S Albert}},
issn = {{1938-2022}},
keywords = {{proteomics; two-dimensional gel electrophoresis; voltage-dependent; anion-selective channel proteins; mitochondria; insulin secretion; mass; spectrometry}},
language = {{eng}},
number = {{5}},
pages = {{283--292}},
publisher = {{Landes Bioscience}},
series = {{Islets}},
title = {{Mitochondrial proteome analysis reveals altered expression of voltage dependent anion channels in pancreatic beta-cells exposed to high glucose}},
url = {{http://dx.doi.org/10.4161/isl.2.5.12639}},
doi = {{10.4161/isl.2.5.12639}},
volume = {{2}},
year = {{2010}},
}