2013 Fiscal Year Final Research Report
Functional analysis of endoplasmic reticulum stress in the progression of cartilage degeneration
| Project/Area Number |
23592219
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
MIZUTA Hiroshi 熊本大学, 大学院生命科学研究部, 教授 (60174025)
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| Co-Investigator(Kenkyū-buntansha) |
HIROSE Jun 熊本大学, 医学部附属病院, 講師 (40433007)
OKADA Tatsuya 熊本大学, 医学部附属病院, 特任助教 (90588401)
TAKADA Koji 熊本大学, 医学部附属病院, 医員 (70599430)
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| Co-Investigator(Renkei-kenkyūsha) |
OYADOMARI Seiichi 徳島大学, 疾患ゲノム研究センター, 教授 (90502534)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 小胞体ストレス / 軟骨変性 / 軟骨細胞 / 小胞体ストレス関連遺伝子 / アポトーシス |
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| Research Abstract |
We investigated the role of proapoptotic transcription factor Chop in murine chondrocyte apoptosis and in the progression of cartilage degeneration, using Chop-knockout (Chop-/-) chondrocytes and model of surgically-induced osteoarthritis (OA) in Chop-/- mice. Our results indicate that Chop plays a direct role in chondrocyte apoptosis and that endoplasmic reticulum (ER) stress-mediated apoptosis contributes to the progression of cartilage degeneration in mice. We also investigated the role of ER stress sensor Perk, Ire1alpha, and Atf6alpha in cartilage degeneration and chondrocyte metabolism with Perk+/-, Ire1alpha+/-, and Atf6alpha-/- mouse models of OA and these genes-knockdown chondrocytes. The results suggest that Atf6alpha involves the progress of cartilage degeneration and the expression of Ire1alpha and Atf6alpha relates with chondrocyte anabolism.
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Research Products
(6 results)
