2013 Fiscal Year Final Research Report
TRPV4, a Ca ion channel plays pivotal role in chondrogenic mechanotransduction in ATDC5
| Project/Area Number |
24659671
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Nagoya University |
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Principal Investigator |
ISHIGURO Naoki 名古屋大学, 医学(系)研究科(研究院), 教授 (20212871)
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| Co-Investigator(Kenkyū-buntansha) |
KITOH Hiroshi 名古屋大学, 医学部附属病院, 准教授 (40291174)
SAKAI Tadahiro 名古屋大学, 医学部附属病院, 病院講師 (60378198)
KANEKO Hiroshi 名古屋大学, 大学院医学系研究科, 寄附講座助教 (60566975)
MISHIMA Kenichi 名古屋大学, 大学院医学系研究科, 寄附講座助教 (40646519)
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| Co-Investigator(Renkei-kenkyūsha) |
NARUSE Keiji 岡山大学, 大学院医歯薬学総合研究科, 教授 (40252233)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Keywords | TRPV4 / SOX9 / 機械的刺激 / 軟骨細胞分化 / ATDC5細胞 |
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| Research Abstract |
It is well known that chondrocyte metabolic activity is partly regulated by physical factors.However, the specific cellular mechanosensor responsible for perception and transduction has not been fully identified in chondrocytes. It has already reported that TRPV4 activation can contribute to the process of chondrogenesis via SOX9 pathway.In this study we demonstrated that TRPV4 works as a mechanoreceptor in response to mechanical stress in chondrocytes, and to determine the intracellular mechanisms leading to the chondorogensis. Our conclusions are as follow, Mechanical stress promoted chondorogensis in ATDC5 cells with increasing mRNA expression of SOX9. Inhibition of TRPV4 by chmical and siRNA suppressed chondrogenesis effect of mechanical stress in ATDC5 cells. Ca influx by mechanical stress was suppressed by RR supplementation and TRPV4 siRNA transfection.
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