Analysis of mechanotransduction mechanism of low magnitude and high frequency loading-induced gain of bone mass.

2015 Fiscal Year Final Research Report

• Project/Area Number: 26861619
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Prosthodontics/ Dental materials science and
• 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)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: メカノトランスダクション / ERK

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.

Free Research Field

歯科補綴学