Analysis of mechanotransduction mechanism of low magnitude and high frequency loading-induced gain of bone mass.
Project/Area Number |
26861619
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Prosthodontics/ Dental materials science and
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Research Institution | Tohoku University |
Principal Investigator |
MATSUI Hiroyuki 東北大学, 東北メディカル・メガバンク機構, 助教 (10547277)
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Project Period (FY) |
2014-04-01 – 2016-03-31
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Project Status |
Completed (Fiscal Year 2015)
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Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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Keywords | メカノトランスダクション / ERK / 骨メカノバイオロジー / JNK / p38 |
Outline of Final Research Achievements |
It is well known that proper mechanical stress induces gain of bone mass while local overloading and unloading results in bone loss. Previously we observed that JNK and p38-activating mechanical stress in osteoblast induced expression of bone resorption-related genes, and low magnitude mechanical stress that preferentially activated ERK pathway induced osteoblast differentiation. However, MAP3K(s) that activate ERK pathway in response to low magnitude mechanical stress remains to be elucidated. In this study, we constructed RNAi screening system that detects potential genes located upstream of ERK pathway, then tested all existing 23 MAP3Ks for screening.
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Report
(3 results)
Research Products
(4 results)
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[Journal Article] The expression of Fn14 via mechanical stress-activated JNK contributes to apoptosis induction in osteoblasts.2014
Author(s)
Matsui, H., Fukuno, N., Kanda, Y., Kantoh, Y., Chida, T., Nagaura, Y., Suzuki, O., Nishitoh, H., Takeda, K., Ichijo, H., Sawada, Y., Sasaki, K., Kobayashi, T. and Tamura, S.
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Journal Title
J. Biol. Chem.
Volume: 289
Issue: 10
Pages: 6438-6450
DOI
Related Report
Peer Reviewed / Open Access
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