2017 Fiscal Year Final Research Report
p21 deficiency was susceptible to osteoarthritis with inflammation.
Project/Area Number |
15K10471
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Orthopaedic surgery
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Research Institution | Kobe University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
林 申也 神戸大学, 医学部附属病院, その他 (20437487)
神崎 至幸 神戸大学, 医学部附属病院, その他 (30514632)
橋本 慎吾 神戸大学, 医学部附属病院, その他 (20457089)
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Project Period (FY) |
2015-04-01 – 2018-03-31
|
Keywords | p21 / 軟骨 / 変形性関節症 |
Outline of Final Research Achievements |
P21 was identified as cell cycle regulator which its induction by p53 during a DNA damage-induced G (1)-phase checkpoint response inhibits both Cyclin-dependent kinase activities.We evaluated synovitis with H-E stain section. At postoperative 1week, both p21(-/-) and WT showed synovial membrane outgrowth. At 8week, synovial inflammation was postponed only in p21(-/-) mice. Macrophage invasion to synovium was analyzed with F4/80 immunohistochemistry showed that. surface linier of synovial membranes were strongly stained in p21(-/-) mice compared with WT at1 or 8week. We evaluated and found that synovial membrane of p21(-/-) mice were strongly stained compared with Wt. Safranin O staining in joint cartilage tissues were evaluated by OARSI histopathology classification. P21(-/-) mice post DMM surgery at 8 weeks showed severe cartilage degeneration. We demonstrated that the p21 deficiency was susceptible to osteoarthritis change with macrophage infiltration to synovial tissues.
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Free Research Field |
整形外科学
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