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葡萄糖诱导的培养血管平滑肌细胞中Na+/H+逆向转运活性和基因表达的变化。蛋白激酶C的作用。

Glucose-induced changes in Na+/H+ antiport activity and gene expression in cultured vascular smooth muscle cells. Role of protein kinase C.

作者信息

Williams B, Howard R L

机构信息

Department of Medicine, University of Leicester School of Medicine, United Kingdom.

出版信息

J Clin Invest. 1994 Jun;93(6):2623-31. doi: 10.1172/JCI117275.

DOI:10.1172/JCI117275
PMID:8201001
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC294501/
Abstract

Increased Na+/H+ antiport activity has been implicated in the pathogenesis of hypertension and vascular disease in diabetes mellitus. The independent effect of elevated extracellular glucose concentrations on Na+/H+ antiport activity in cultured rat vascular smooth muscle cells (VSMC) was thus examined. Amiloride-sensitive 22Na+ uptake by VSMC significantly increased twofold after 3 and 24 h of exposure to high glucose medium (20 mM) vs. control medium (5 mM). Direct glucose-induced Na+/H+ antiport activation was confirmed by measuring Na(+)-dependent intracellular pH recovery from intracellular acidosis. High glucose significantly increased protein kinase C (PKC) activity in VSMC and inhibition of PKC activation with H-7, staurosporine, or prior PKC downregulation prevented glucose-induced increases in Na+/H+ antiport activity in VSMC. Northern analysis of VSMC poly A+ RNA revealed that high glucose induced a threefold increase in Na+/H+ antiport (NHE-1) mRNA at 24 h. Inhibiting this increase in NHE-1 mRNA with actinomycin D prevented the sustained glucose-induced increase in Na+/H+ antiport activity. In conclusion, elevated glucose concentrations significantly influence vascular Na+/H+ antiport activity via glucose-induced PKC dependent mechanisms, thereby providing a biochemical basis for increased Na+/H+ antiport activity in the vascular tissues of patients with hypertension and diabetes mellitus.

摘要

钠/氢逆向转运活性增加与糖尿病患者高血压和血管疾病的发病机制有关。因此，研究了细胞外葡萄糖浓度升高对培养的大鼠血管平滑肌细胞（VSMC）中钠/氢逆向转运活性的独立影响。与对照培养基（5 mM）相比，VSMC对氨氯地平敏感的22Na+摄取在暴露于高葡萄糖培养基（20 mM）3小时和24小时后显著增加了两倍。通过测量细胞内酸中毒后钠依赖性细胞内pH恢复，证实了直接葡萄糖诱导的钠/氢逆向转运激活。高葡萄糖显著增加了VSMC中的蛋白激酶C（PKC）活性，用H-7、星形孢菌素抑制PKC激活或预先下调PKC可防止葡萄糖诱导的VSMC中钠/氢逆向转运活性增加。对VSMC多聚A+RNA的Northern分析显示，高葡萄糖在24小时时使钠/氢逆向转运（NHE-1）mRNA增加了三倍。用放线菌素D抑制NHE-1 mRNA的这种增加可防止葡萄糖诱导的钠/氢逆向转运活性持续增加。总之，葡萄糖浓度升高通过葡萄糖诱导的PKC依赖性机制显著影响血管钠/氢逆向转运活性，从而为高血压和糖尿病患者血管组织中钠/氢逆向转运活性增加提供了生化基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/294501/2025eb87a97f/jcinvest00035-0336-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/294501/26f7ab183624/jcinvest00035-0333-a.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/294501/2025eb87a97f/jcinvest00035-0336-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/294501/26f7ab183624/jcinvest00035-0333-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/294501/d17a578aeb05/jcinvest00035-0333-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/294501/4fc941f9cd98/jcinvest00035-0336-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/294501/03cb3f58f84e/jcinvest00035-0336-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dcc/294501/2025eb87a97f/jcinvest00035-0336-c.jpg

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