Glucose enhances expression of TRPC1 and calcium entry in endothelial cells
Glucose enhances expression of TRPC1 and calcium entry in endothelial cells
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DOI：
10.1152/ajpheart.00699.2009
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发表时间：
2010-01-01
影响因子：
4.8
通讯作者：
Ding, H.
中科院分区：
文献类型：
--
作者：
Bishara, N. B.;Ding, H.
葡萄糖对内皮细胞TRPC1表达和钙进入的影响。[J] .中华心脏杂志，2016,31(1):1- 3。首次发表于2009年10月23日；doi: 10.1152 / ajpheart.00699.2009。高血糖是内皮功能障碍和血管疾病的主要危险因素，在目前的研究中，在高糖（HG; 25mmol /l）和低糖（LG; 5.5 mmol/l；对照）的牛主动脉内皮细胞中，探讨了葡萄糖诱导的细胞内Ca2+ (Ca-i(2+))异常稳态的联系。与LG相比，HG在72 h时瞬时受体电位1 （TRPC1）离子通道蛋白的表达显著增加，但TRPC3、TRPC4和TRPC6的表达没有显著增加。HG在4、24和72 h时没有改变基础Ca-i（2+）或atp诱导的Ca-i（2+）释放；然而，持续Ca-i（2+）的振幅在24和72 h显著增加，并被低浓度的非特异性TRPC阻滞剂钆、SKF-96365和2-氨基乙氧基二苯硼酸盐降低。TRPC1反义处理显著降低TRPC1蛋白表达和atp诱导的牛主动脉内皮细胞Ca2+进入。虽然HG诱导的TRPC1表达变化、Ca2+进入增强和内皮功能障碍之间的联系需要进一步研究，但目前的数据表明，靶向这些途径可能会降低HG对内皮功能的影响。
Bishara NB, Ding H. Glucose enhances expression of TRPC1 and calcium entry in endothelial cells. Am J Physiol Heart Circ Physiol 298: H171-H178, 2010. First published October 23, 2009; doi:10.1152/ajpheart.00699.2009.-Hyperglycemia is a major risk factor for endothelial dysfunction and vascular disease, and in the current study, the link to glucose-induced abnormal intracellular Ca2+ (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 Ca2+ entry in bovine aortic endothelial cells. Although the link between HG-induced changes in TRPC1 expression, enhanced Ca2+ 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.