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Mesenteric vascular remodeling in hyperhomocysteinemia.

C Munjal¹, S Givvimani, N Qipshidze

¹Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY 40202, USA.

Molecular and Cellular Biochemistry

|November 16, 2010

Summary

Hyperhomocysteinemia (HHcy) in mice activates matrix metalloproteinase-9 (MMP-9), reduces nitric oxide (NO) production, and causes mesenteric artery remodeling, leading to hypertension. MMP-9 inhibition prevented HHcy-induced blood pressure increase.

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Area of Science:

Vascular Biology
Cardiovascular Physiology
Biochemistry

Background:

Vascular remodeling involves extracellular matrix synthesis and degradation, regulated by matrix metalloproteinases (MMPs).
Nitric oxide (NO) typically keeps vascular MMPs latent, but oxidative stress can activate them, instigating remodeling.
Hyperhomocysteinemia (HHcy) reduces NO bioavailability, potentially activating MMPs and causing vascular dysfunction.

Purpose of the Study:

To investigate the hypothesis that HHcy decreases NO bioavailability by activating MMPs, reducing elastin, dimethylarginine dimethylaminohydrolase-2 (DDAH-2), and endothelial nitric oxide synthase (eNOS), while increasing connexin expression.
To determine the role of MMP-9 in HHcy-induced mesenteric artery remodeling and hypertension.

Main Methods:

Utilized 12-week-old wild-type (WT) and cystathione beta synthase heterozygote knockout (CBS+/-) mice to model HHcy.

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Administered homocysteine (Hcy) to WT and MMP-9 knockout mice; measured blood pressure via radio-telemetry.

Analyzed superior mesenteric artery and arcade using microscopy; quantified protein and mRNA expression (MMP-9, DDAH-2, eNOS, connexin-40) via Western blot and RT-PCR.

Main Results:

CBS+/- mice exhibited decreased DDAH-2 and eNOS expression compared to WT mice.
Mesenteric arteries of CBS+/- mice showed increased MMP-9 and connexin-40 expression and wall thickness.
Hcy treatment increased blood pressure in WT mice, but not in MMP-9 knockout mice, indicating MMP-9's role in hypertension.

Conclusions:

HHcy induces mesenteric artery remodeling and narrowing by activating MMP-9 and decreasing DDAH-2 and eNOS, compromising blood flow.
This remodeling contributes to hypertension and potentially acute abdominal pain.
MMP-9 is a key mediator in HHcy-induced hypertension.