Glucose enhances expression of TRPC1 and calcium entry in endothelial cells

N. B. Bishara, Hong Ding

Research output: Contribution to journalArticle

30 Citations (Scopus)


Hyperglycemia is a major risk factor for endothelial dysfunction and vascular disease, and in the current study, the link to glucose-induced abnormal intracellular Ca 2+ (Ca i 2+ ) homeostasis was explored in bovine aortic endothelial cells in high glucose (HG; 25 mmol/l) versus low glucose (LG; 5.5 mmol/l; control). Transient receptor potential 1 (TRPC1) ion channel protein, but not TRPC3, TRPC4, or TRPC6 expression, was significantly increased in HG versus LG at 72 h. HG for 4, 24, and 72 h did not change basal Ca i 2+ or ATP-induced Ca i 2+ release; however, the amplitude of sustained Ca i 2+ was significantly increased at 24 and 72 h and reduced by low concentration of the putative, but nonspecific, TRPC blockers, gadolinium, SKF-96365, and 2-aminoethoxydiphenyl borate. Treatment with TRPC1 antisense significantly reduced TRPC1 protein expression and ATP-induced Ca 2+ entry in bovine aortic endothelial cells. Although the link between HG-induced changes in TRPC1 expression, enhanced Ca 2+ entry, and endothelial dysfunction require further study, the current data are suggestive that targeting these pathways may reduce the impact of HG on endothelial function.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number1
Publication statusPublished - Jan 2010



  • Bovine aorta endothelial cells
  • Diabetes
  • Endothelial dysfunction
  • Hyperglycemia
  • Store-operated calcium entry
  • Transient receptor potential channel antisense
  • Transient receptor potential channels

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

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