Ang-II-induced Ca2+ influx is mediated by the 1/4/5 subgroup of the transient receptor potential proteins in cultured aortic smooth muscle cells from diabetic Goto-Kakizaki rats

作者：Evans Jodi F; Lee Jin Hee; Ragolia Louis^*

来源：Molecular and Cellular Endocrinology, 2009, 302(1): 49-57.

DOI：10.1016/j.mce.2008.12.004

• Goto-Kakizaki
• Diabetes
• Transient receptor potential canonical (TRPC)
• Calcium
• Vascular smooth muscle cells (VSMCs)

Angiotensin-II (Ang-II) exerts many of its vascular effects, including the pathophysiological changes associated with type 2 diabetes, through changes in intracellular calcium concentration [Ca2+](i). We sought to clarify the mechanism responsible for Ang-II-induced Ca2+ influx in cultured aortic VSMC using the Goto-Kakizaki (GK) rat model of type 2 diabetes. Ang-II-induced Ca2+ influx was blocked by neither VDCC nor c-src inhibition but was sensitive to inositol 1,4,5-trisphosphate receptor inhibition, lanthanide and the diacylglycerol analogue, oleoyl-2-acetyl-sn-glycerol. Since transient receptor potential canonical (TRPC)3 gene expression was undetectable in both WKY and GK VSMCs and TRPC6 gene and protein expression were significantly down-regulated in GK, we believe the 1/4/5 subgroup of TRPC proteins plays a significant role. Furthermore, in GK VSMC the elevated calcium influx observed was not attributable to increased TRPC expression, but rather an alteration of TRPC activity.

• 出版日期2009-4-10