| Title | Glucose enhances expression of TRPC1 and Ca entry in endothelial cells. | | Author(s) | Bishara NB, Ding H | | Institution | RMIT. | | Source | Am J Physiol Heart Circ Physiol 2009 Oct 23. | | 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. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 19855058 |
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