| Project/Area Number |
25670651
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Hiroshima University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKASA Tomoyuki 広島大学, 病院, 病院助教 (60467769)
KATO Yoshio 独立行政法人産業技術総合研究所, バイオメディカル研究部門, 研究員 (20415657)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 変形性関節症 / 酸化ストレス / ヘムオキシゲナーゼ-１ / SOD2 / 軟骨細胞 / アポトーシス / 軟骨 / 抗酸化 / ジンクフィンガープロテイン / HO-1 / microRNA |
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| Outline of Final Research Achievements |
Bach1 is a transcriptional repressor of Heme oxygenase-1 (HO-1), which is cytoprotective through its antioxidant effects. The objective of this study was to define the role of HO-1 in osteoarthritis (OA) development using in Bach1 deficient mice. HO-1 expression decreased with aging in articular cartilages. Bach1 deficient mice showed reduced severity of age-related OA and surgically-induced OA compared with wild-type mice. Autophagy marker LC3 and antioxidant SOD2 were increased in articular cartilage of Bach1 deficient mice compared with wild-type mice. The expression of SOD2 and the suppression of apoptosis in Bach1 deficient chondrocytes were mediated by HO-1. This may be due to maintenance of joint health by antioxidant effects through HO-1. These results suggest that HO-1 or inactivation of Bach1 is a novel target and signal pathway in OA prevention.
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