The Expression of L-type Calcium Channel mRNA by the Concentrations of Glucose on the Cell Proliferation in Cultured OLETF Rat Aortic Vascular Smooth Muscle Cells.
- Author:
Hyung Joon YOO
;
Young Jung CHO
;
Hong Woo NAM
- Publication Type:Original Article
- MeSH:
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester;
Animals;
Aorta;
Calcium Channels, L-Type*;
Cell Proliferation*;
Culture Media;
Glucose*;
Muscle, Smooth, Vascular*;
Rats;
Rats, Inbred OLETF*;
RNA, Messenger*;
Verapamil
- From:Journal of the Korean Geriatrics Society
2004;8(4):191-195
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The proliferation of vascular smooth muscle cell(VSMC) is a part of the major pathogenic mechanism for atheroscle- rosis. It has been reported that L-type calcium channel plays a role in the VSMC proliferation in diabetic rats. But there is a little study results about the association between L-type calcium channel and VSMC proliferation by glucose concentrations in culture media. So we examined the association between voltage-dependent L-type calcium channel of VSMCs and the proliferative activity of vascular smooth muscle cells. METHODS: Rat aortic VSMCs were isolated from the aorta of OLETF rat by enzyme method. VSMCs were cultured in various concentrations of glucose(5.5, 25 mM). The VSMCs(1x104 cells in 24-well plates) were incubated in the presence of Bay K 8644 (10-6M) with/without verapamil(10-6M) for 48 hours. Then the proliferation was assessed by MTT(methylthiazole tetrazolium) assay and expression of L-type calcium channel mRNA was measured by RT-PCR. RESULTS: The proliferative ability and the expression of L-type calcium channel of cultured VSMCs were increased dose-dependently by the glucose concentrations(p<0.05). Bay K 8644 enhanced the proliferation of VSMC and verapamil blocked the incremental effects induced by Bay K 8644. CONCLUSION: These results suggest that L-type calcium channel may play a role in VSMC proliferation of OLETF rat.