Activation of the hypoxia-inducible factor-1 in overloaded temporomandibular joint, and induction of osteoclastogenesis

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• 作者：Maya Shirakura ; Keiji Tanimoto ; Hidetaka Eguchi ; Mutsumi Miyauchi ; Hideaki Nakamura ; Keiko Hiyama ; Kotaro Tanimoto ; Eiji Tanaka ; Takashi Takata ; Kazuo Tanne
• 关键词：Temporomandibular joint (TMJ) ; Osteoarthritis (OA) ; Chondrocyte ; Hypoxia-inducible factor-1 (Hif-1) ; Osteoprotegerin (Opg)
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2010
• 出版时间：19 March 2010
• 年：2010
• 卷：393
• 期：4
• 页码：800-805
• 全文大小：669 K

文摘

Vascular endothelial growth factor (Vegf) was previously shown to be expressed specifically in the condylar cartilage of temporomandibular joint-osteoarthritis (TMJ-OA) model rats. Here we demonstrate for the first time that hypoxia-inducible factor-1α (Hif-1α) is activated in mature chondrocytes of temporomandibular joint-osteoarthritis (TMJ-OA) model rat by mechanical overload, and that activated Hif-1 in chondrocytes can induce osteoclastogenesis via repression of osteoprotegerin (Opg) expression.

In rat TMJs, degeneration of the condylar cartilage became prominent in proportion to the duration of overloading. Hif-1α expression was observed specifically in mature and hypertrophic chondrocytes, and Hif-1α-positivity, level of Vegf expression, and tartrate-resistant acid phosphatase (TRAP)-positive cell numbers all increased in the same manner. When ATDC5 cells induced differentiation by insulin were cultured under hypoxia, Hif-1α induction was observed in mature stage, but not in immature stage. Inductions of Hif-1-target genes showed a similar expression pattern. In addition, expression of Opg decreased in hypoxia, and Hif-1α played a role, in part, in its regulation.