Effects of hypoxia/ischemia on catabolic mediators of cartilage in a human chondrocyte, SW1353
- Effects of hypoxia/ischemia on catabolic mediators of cartilage in a human chondrocyte, SW1353
- 홍영훈; 박찬원; 김희선; 원규장; 김용운; 이충기
- INDUCIBLE FACTOR-I; ARTICULAR CHONDROCYTES; NITRIC-OXIDE; INTERLEUKIN-8 EXPRESSION; GLUCOSE-CONCENTRATION; OXYGEN-CONSUMPTION; GROWTH-FACTOR; HYPOXIA; CELLS; HIF-1-ALPHA
- Issue Date
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.431, no.3, pp.478 - 483
- Cells from a human chondrocyte cell line were studied in 1% oxygen and/or a lower glucose concentration (5.5 mM), compared to the routine culture conditions of normoxia and high glucose. HIF-1 alpha, IL-1 beta, IL-6, IL-8, COX-2, TNF alpha, LIF, MMP-3, MMP-13, and reactive oxygen species (ROS) were evaluated, respectively. Effects of hypoxia inducing expression of HIF-1 alpha were statistically significant at 72 h (p < 0.05). Increased production of ROS by hypoxia was also observed with passage of time (p < 0.05). The effects of hypoxia on HIF-1 alpha and IL-1 beta were potentiated by 5.5 mM glucose, especially after 48 h (p < 0.05). IL-8 production was significantly induced in 1% O-2, with 5.5 mM glucose (p < 0.01). IL-8 mRNA expression and production in response to IL-1 beta were potentiated by hypoxia/ischemia (p < 0.05, p < 0.01, respectively). Up-regulation of IL-1 beta, ROS, and IL-8 by hypoxia/ischemia in human chondrocytes may occur in correlation with HIF-1 alpha. IL-8 response to IL-1 beta may be potentiated synergically by hypoxia/ischemia, as an effector of hypoxia/ischemia. The results may suggest aggressive biology of the ordinary cartilage hypoxia/ischemia in the context of arthro-degeneration. (C) 2013 Elsevier Inc. All rights reserved.
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