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Related Experiment Video

Updated: May 8, 2026

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion

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In vivo effect of insulin to decrease matrix metalloproteinase-2 and -9 activity after arterial injury.

June Guo¹, Jiwanjeet K Dhaliwall, Kalam K Chan

¹Department of Physiology, University of Toronto, Toronto, Ont., Canada.

Journal of Vascular Research

|August 31, 2013

Summary

Insulin treatment significantly reduced matrix metalloproteinase (MMP) activity and expression in rats after arterial injury. This finding supports insulin's protective role in blood vessel health by inhibiting smooth muscle cell migration.

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Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion

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Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function

Published on: June 11, 2017

Area of Science:

Cardiovascular Biology
Endocrinology
Molecular Medicine

Background:

In vitro studies show insulin promotes growth and protects blood vessels.
In vivo, insulin primarily exhibits protective effects on vasculature.
Smooth muscle cell (SMC) migration and neointimal growth are key factors in vascular injury response.

Purpose of the Study:

To investigate the impact of normoglycemic hyperinsulinemia on matrix metalloproteinase (MMP) activity following balloon angioplasty.
To elucidate the mechanism behind insulin's vasculoprotective effects in vivo.

Main Methods:

Rats underwent carotid angioplasty and were divided into control and insulin-treated groups.
Normoglycemia was maintained using oral glucose administration.
Matrix metalloproteinase activity and expression (mRNA and protein) were assessed using gelatin zymography and other molecular techniques.

Main Results:

Insulin treatment significantly reduced the gelatinolytic activity of pro-MMP-2, MMP-2, and MMP-9 by 44-51% compared to controls.
Insulin decreased both mRNA and protein levels of MMP-2 and MMP-9.
No significant changes were observed in membrane-type 1 MMP or tissue inhibitors of MMP activity.

Conclusions:

Insulin effectively inhibits key matrix metalloproteinases involved in extracellular matrix degradation after arterial injury.
These findings suggest a mechanism where insulin suppresses SMC migration, thereby supporting its role in vasculoprotection.
The study highlights the therapeutic potential of insulin in managing vascular complications.