Nifedipine decreases sVCAM-1 concentrations and oxidative stress in systemic sclerosis

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Arthritis Research & Therapy

12 May 2004

Research article

Nifedipine decreases sVCAM-1 concentrations and oxidative stress in

systemic sclerosis but does not affect the concentrations of vascular

endothelial growth factor or its soluble receptor 1

Yannick Allanore1 , Didier Borderie2, Hervé Lemaréchal2, Ohvanesse

Garabed Ekindjian2 and André Kahan1

1Paris V University, Department of Rheumatology A, Assistance Publique

Hôpitaux de Paris, Cochin Hospital, Paris, France

2Department of Biochemistry A, Assistance Publique Hôpitaux de Paris,

Cochin Hospital, Paris, France

Abstract

Microvascular injury, oxidative stress, and impaired angiogenesis are

prominent features of systemic sclerosis (SSc). We compared serum

markers of these phenomena at baseline and after treatment with

nifedipine in SSc patients. Forty successive SSc patients were compared

with 20 matched healthy subjects. All SSc patients stopped taking

calcium-channel blockers 72 hours before measurements. Twenty SSc

patients were also examined after 14 days of treatment with nifedipine

(60 mg/day). Quantitative ELISA was used to measure the serum

concentrations of vascular endothelial growth factor (VEGF), soluble

VEGF receptor 1 (sVEGFR-1), soluble vascular cell adhesion molecule 1

(sVCAM-1), carbonyl residues, and advanced oxidation protein products

(AOPP). The median concentrations of VEGF, sVEGFR-1, sVCAM-1, carbonyl

residues, and AOPP were significantly higher in SSc patients than in

healthy subjects at baseline. A correlation was found between VEGF

concentration and carbonyl residue concentration (r = 0.43; P = 0.007).

Nifedipine treatment led to a significant decrease in concentrations of

sVCAM-1, carbonyl residues, and AOPP but did not affect concentrations

of VEGF and sVEGFR-1. Nifedipine treatment ameliorated endothelium

injury in patients with SSc, as shown by the concentrations of adhesion

molecules and oxidative damage markers. The fact that VEGF and sVEGFR-1

concentrations were not changed whereas oxidative stress was ameliorated

by nifedipine is consistent with the hypothesis that VEGF signalling is

impaired in SSc. However, more experimental evidence is needed to

determine whether the VEGF pathway is intrinsically defective in SSc.

http://arthritis-research.com/content/6/4/R309/abstract

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