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Nitric Oxide Signaling Pathway

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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...

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Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery

Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery

Published on: December 23, 2014

The effect of insulin to decrease neointimal growth after arterial injury is endothelial nitric oxide

June Guo¹, Danna M Breen¹, Troy J Pereira²

¹Department of Physiology, University of Toronto, Toronto, ON M5S 1A8, Canada.

Atherosclerosis

|May 15, 2015

Summary

Insulin

Keywords:

Angioplasty Endothelial nitric oxide synthase Insulin Neointima Re-endothelialization

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Published on: June 11, 2017

Area of Science:

Vascular biology
Endocrinology
Cardiovascular research

Background:

Insulin exhibits dual effects on vascular cells in vitro: mitogenic on smooth muscle cells and protective on endothelial cells.
Insulin stimulates nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) expression, crucial for vascular health.
Previous in vivo studies demonstrated insulin's ability to reduce neointimal growth and enhance re-endothelialization after arterial injury.

Purpose of the Study:

To investigate the role of nitric oxide synthase (NOS), specifically eNOS, in mediating insulin's vasculoprotective effects in vivo.
To determine if the beneficial effects of insulin on neointimal formation and re-endothelialization are dependent on NOS activity.

Main Methods:

Rats received insulin implants with or without the NOS inhibitor l-NAME before arterial balloon injury.
Insulin's effects on neointimal area, cell migration, and re-endothelialization were assessed.
Wild-type and eNOS knockout mice were treated with insulin to evaluate neointimal formation after femoral artery injury.

Main Results:

Insulin significantly reduced neointimal area and cell migration while increasing re-endothelialization in rats.
Co-administration of l-NAME abolished all beneficial effects of insulin, indicating a critical role for NOS.
Insulin increased eNOS phosphorylation and improved endothelial-dependent vasorelaxation.
Insulin's protective effect against neointimal formation was observed in wild-type mice but absent in eNOS knockout mice.

Conclusions:

The vasculoprotective effects of insulin following arterial injury are critically dependent on the endothelial nitric oxide synthase (eNOS) pathway.
Insulin promotes vascular healing through an eNOS-dependent mechanism, highlighting its therapeutic potential in cardiovascular diseases.