Glucose enhances expression of TRPC1 and calcium entry in endothelial cells

Bishara, N and Ding, H 2009, 'Glucose enhances expression of TRPC1 and calcium entry in endothelial cells', American journal of physiology heart and circulatory physiology, vol. 298, pp. 171-178.


Document type: Journal Article
Collection: Journal Articles

Title Glucose enhances expression of TRPC1 and calcium entry in endothelial cells
Author(s) Bishara, N
Ding, H
Year 2009
Journal name American journal of physiology heart and circulatory physiology
Volume number 298
Start page 171
End page 178
Total pages 8
Publisher American Physiological society
Abstract Hyperglycemia is a major risk factor for endothelial dysfunction and vascular disease and, in the current study, the link to glucose-induced abnormal intracellular calcium (Ca(2+)i) homeostasis was explored in bovine aortic endothelial cells (BAECs) in high glucose (HG) (25 mmol/L) versus control (low glucose, LG) (5.5 mmol/L). Transient receptor potential 1 (TRPC1) ion channel protein, but not TRPC3, TRPC4 or TRPC6 expression, was significantly increased in HG vs. LG at 72 h. HG for 4, 24 and 72 h did not change basal Ca(2+)i or ATP-induced Ca(2+)i release, however, the amplitude of sustained Ca(2+)i was significantly increased at 24 and 72 h and reduced by low concentration of the putative, but non-specific, TRPC blockers, gadolinium (Gd(3+)), SKF96365 and 2-aminoethoxydiphenyl borate (2-APB). Treatment with TRPC1 antisense significantly reduced TRPC1 protein expression and ATP-induced Ca(2+) entry in BAECs. Although the link between HG-induced changes in TRPC1 expression, enhanced Ca(2+) entry and endothelial dysfunction requires further study, the current data are suggestive that targeting these pathways may reduce the impact of HG on endothelial function. Key words: Bovine aorta endothelial cells, hyperglycemia, transient receptor potential channels, store-operated calcium entry.
Keyword(s) bovine aorta endothelial cells
hyperglycemia
endothelial dysfunction
diabetes
DOI - identifier 10.1152/ajpheart.00699.2009
Copyright notice American Physiological society 2009
ISSN 1522-1539
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