Nuclear Factor-B Induction by Visfatin in Human Vascular Endothelial Cells:Its role in MMP-2/9 production and activation  

Oleh:

Adya, Raghu ; Tan, Bee K. ; Jing, Chen ; Randeva, Harpal S.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 31 no. 04 (Apr. 2008), page 758.
Topik: HUVEC; human umbilical vein endothelial cell ; MMP; matrix metalloproteinase ; NF-B; nuclear factor-B ; TNF-; tumor necrosis factor-

Ketersediaan

Perpustakaan FK Nomor Panggil: D05.K.2008.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

OBJECTIVE—Visfatin is elevated in obesity and type 2 diabetes and is thought to be an inflammatory mediator within atherosclerotic lesions and to induce gelatinase activity. We investigated the activation of nuclear factor-B (NF-B), a well-known proinflammatory transcription factor, by visfatin in endothelial cells. RESEARCH DESIGN AND METHODS—Human endothelial cells were transfected with pNF-B-Luc plasmid. Using quantitative PCR, Western blot analysis, and gelatin zymography, we studied NF-B signaling in gelatinase-mediated vascular inflammation by visfatin using the NF-B inhibitor BAY 11-7085. RESULTS—Visfatin significantly increased NF-B transcriptional activity (P < 0.001). We also found a significant inhibition of tumor necrosis factor- (TNF-)-induced NF-B activity by visfatin (P < 0.001). Furthermore, the NF-B inhibitor significantly negated visfatin-induced matrix metalloproteinase (MMP)-2/9 mRNA expression, protein levels, and gelatinolytic activity (P < 0.001). CONCLUSIONS—Visfatin-induced NF-B signaling in human endothelial cells affects the activation of gelatinases MMP-2 and -9, suggesting an important role of visfatin in the pathogenesis of vascular inflammation in obesity and type 2 diabetes.

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