Journal of Applied Physiology
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J Appl Physiol 91: 1380-1386, 2001;
8750-7587/01 $5.00
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Vol. 91, Issue 3, 1380-1386, September 2001

Mechanism of inhibition of matrix metalloproteinase-9 induction by NO in vascular smooth muscle cells

Milind V. Gurjar, Jason DeLeon, Ram V. Sharma, and Ramesh C. Bhalla

Department of Anatomy and Cell Biology, The University of Iowa College of Medicine, Iowa City, Iowa 52242

Vascular smooth muscle (VSM) cell migration is a critical step in the development of a neointima after angioplasty. Matrix metalloproteinases (MMPs) degrade the basement membrane and extracellular matrix, facilitating VSM cell migration. Recently, we demonstrated that nitric oxide (NO) inhibits interleukin-1beta (IL-1beta )-stimulated MMP-9 induction in rat aortic VSM cells. In this study, we examined the hypothesis that NO inhibits MMP-9 induction by attenuating superoxide generation and extracellular signal-regulated kinase (ERK) activation. Stimulation of VSM cells with IL-1beta significantly (P < 0.05) increased superoxide production, ERK activation, and MMP-9 induction. Pretreatment of VSM cells with the NO donor DETA NONOate significantly (P < 0.05) decreased IL-1beta -stimulated superoxide generation. In addition, pretreatment of VSM cells with a specific ERK pathway inhibitor, PD-98059, or DETA NONOate inhibited IL-1beta -stimulated ERK activation and MMP-9 induction. Direct exposure of VSM cells to increased superoxide levels by treatment with xanthine/xanthine oxidase increased ERK activation and MMP-9 induction, whereas pretreatment of cells with PD-98059 significantly (P < 0.05) inhibited xanthine/xanthine oxidase-stimulated ERK activation and MMP-9 induction. We conclude that NO inhibits IL-1beta -stimulated MMP-9 induction by inhibiting superoxide generation and subsequent ERK activation.

reactive oxygen species; matrix metalloproteinases; extracellular signal-regulated kinase; vascular smooth muscle cells; interleukin-1beta ; nitric oxide


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