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Diabetes Care Publish Ahead of Print published online ahead of print January 9, 2008
DOI: 10.2337/dc07-1544
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Original Research

Nuclear Factor–{kappa}B Induction by Visfatin in Human Vascular Endothelial Cells: Role in MMP-2/9 Production and Activation

Raghu Adya, MBBS, MSc1, Bee K Tan, MBBS1, Jing Chen, PhD1 and Harpal S Randeva, MBChB, FRCP, MD, PhD1

1Endocrinology & Metabolism Group, Clinical Sciences Research Institute, Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK

Harpal.Randeva{at}warwick.ac.uk

ABSTRACT

Objective: Visfatin is elevated in obesity and T2DM; and thought to be an inflammatory mediator within atherosclerotic lesions inducing gelatinase activity. We investigated the activation of NF-{kappa}B a well-known pro-inflammatory transcription factor by visfatin in ECs.

Research Design and Methods: Human ECs were transfected with pNF-{kappa}B-Luc plasmid. Using Quantitative PCR, western blot analysis and gelatin zymography, we studied NF-{kappa}B signalling in gelatinase mediated vascular inflammation by visfatin; employing the NF-kB inhibitor, BAY 11-7085.

Results: Visfatin significantly increased NF-{kappa}B transcriptional activity (P<0.001). Also, we found a significant inhibition of TNF{alpha} induced NF-{kappa}B activity by visfatin (P<0.001). Furthermore, the NF-{kappa}B inhibitor, significantly negated visfatin induced MMP-2/9 mRNA expression, protein levels, and gelatinolytic activity (P<0.001).

Conclusions: Visfatin induced NF-{kappa}B signalling in human ECs affects the activation of gelatinases-MMP-2/9, suggesting an important role of visfatin in the pathogenesis of vascular inflammation in obesity and T2DM.


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