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Title: Oxidized LDL binding to LOX-1 upregulates VEGF expression in cultured bovine chondrocytes through activation of PPAR-{gamma}

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [1];  [1];  [2];  [2];  [3];  [2];  [1]
  1. Department of Orthopaedic Surgery, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama City, Osaka, 589-8511 (Japan)
  2. Department of Biochemistry, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama City, Osaka, 589-8511 (Japan)
  3. Department of Bioscience, National Cardiovascular Center Research Institute, 5-7-1 Fujishirodai, Suita City, Osaka, 565-8565 (Japan)

It has been reported that vascular endothelial growth factor (VEGF) and its receptors play an important role in the destruction of articular cartilage in osteoarthritis through increased production of matrix metalloproteinases. We investigated whether the oxidized low-density lipoprotein (ox-LDL) binding to lectin-like ox-LDL receptor-1 (LOX-1) upregulates VEGF expression in cultured bovine articular chondrocytes (BACs). Ox-LDL markedly increased VEGF mRNA expression and protein release in time- and dose-dependent manners, which was significantly suppressed by anti-LOX-1 antibody pretreatment. Activation of peroxisome proliferator-activated receptor (PPAR)-{gamma} was evident in BACs with ox-LDL addition and was attenuated by anti-LOX-1 antibody. The specific PPAR-{gamma} inhibitor GW9662 suppressed ox-LDL-induced VEGF expression. These results suggest that the ox-LDL/LOX-1 system upregulates VEGF expression in articular cartilage, at least in part, through activation of PPAR-{gamma} and supports the hypothesis that ox-LDL is involved in cartilage degradation via LOX-1.

OSTI ID:
20854488
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 348, Issue 3; Other Information: DOI: 10.1016/j.bbrc.2006.07.133; PII: S0006-291X(06)01710-4; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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