Inhibition of the Proliferation of Smooth Muscle Cells From Human Coronary Bypass Vessels by Vasonatrin Peptide

Title:

Inhibition of the Proliferation of Smooth Muscle Cells From Human Coronary Bypass Vessels by Vasonatrin Peptide

Creator:

Lu, S.Y., Zhu, M.Z., Wang, D.S., Xhen, S.Y., Zhang, W.D., Dong, H., Yu, J., and Guo, H.T.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:f21a4660-c2aa-4c29-bae3-31dfdbd6baf7
uuid:f21a4660-c2aa-4c29-bae3-31dfdbd6baf7

Subject:

Vasonatrin peptide, Vascular smooth muscle cells, and Proliferation

Type:

article, model:article, and TEXT

Description:

Abnormal proliferation of vascular smooth muscle cells (VSMCs) is known to be a key event in the development of atherosclerosis and restenosis. The present study examined the effect of a novel synthetic natriuretic peptide, vasonatrin peptide (VNP), on norepinephrine (NE)-induced proliferation of VSMCs from coronary bypass vessels. Human VSMCs were isolated from an internal mammary artery (IMA) and saphenous vein (SV) by explant culture and stimulated with NE. MTT assay and [3H] thymidine-incorporation were undertaken to analyze cell proliferation and radioimmunoassay was used to determine the level of intracellular cyclic 3’,5’-guanosine monophosphate (cyclic GMP). NE (10-8 - 10-7 mol/l) had a mitogenic effect in human VSMCs from both SV and IMA. However, NE-stimulated proliferation of VSMCs from SV was greater than that from IMA. Furthermore, low concentration of NE (10-10 mol/l) promoted cell growth in SV-derived cells but not in IMA-derived cells. VNP (10-8 - 10-6 mol/l) reduced NE-induced cell proliferation and increased intracellular cyclic GMP, which were abrogated by HS-142-1. In addition, the growth inhibition of VNP was mimicked by 8-bromo-cGMP. These results indicate that VNP has a significant inhibitory effect on NE-stimulated proliferation of human VSMCs from both IMA and SV, which is mediated by guanylate cyclase-linked receptors by increasing cyclic GMP.

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2004 Volume:53 | Number:4

Harvested from:

CDK

Metadata only:

false