2013 Fiscal Year Final Research Report
Investigation of the molecular mechanism of osteoclast function
| Project/Area Number |
23590374
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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 |
Pathological medical chemistry
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| Research Institution | Himeji Dokkyo University |
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Principal Investigator |
TOHYAMA Yumi 姫路獨協大学, 薬学部, 教授 (70362770)
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| Co-Investigator(Renkei-kenkyūsha) |
KAJI Hiroaki 姫路獨協大学, 薬学部, 講師 (10368706)
TANAKA Chisato 姫路獨協大学, 薬学部, 助手 (30461122)
MORITA Hiroyuki 姫路獨協大学, 薬学部, 助手 (90648594)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 破骨細胞 |
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| Research Abstract |
To determine the molecular mechanism of osteoclast activation, human monocytes and human leukemic cell line, HL60 were used after differentiation into ostelclast-like cells. To analyze the role of target molecules on osteoclast function, knocked down cells of PKC-delta, KIF20A, Vimentin, or SMN, were established by lentiviral transfection containing each shRNA. Knockdown of PKC-delta or Vimentin led to decreased podosome (F-actin structure) formation. Knockdown of both KIF20A and SMN increased multinuclear cells resulting from cell to cell fusion. In addition, SMN-knockdown promoted alpha-tubulin acetylation (K40), which is essential for lysosomal trasnport, suggesting that SMN is a regulator of osteoclast activation.
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[Journal Article] Rab27b regulates c-kit expression by controlling the secretion of stem cell factor2012
Author(s)
Tanaka C, Kaji H, He J, Hazama R, Yokoyama K, Kinoshita E, Tsujioka T, Tohyama K, Yamamura H, Nishio H, Tohyama Y
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Journal Title
Biochem Biophys Res Commun
Volume: 419
Pages: 368-373
DOI
Peer Reviewed
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