Mechanical stress induces the activation of TAK1 and its downstream pathways in pre-osteoblastic cells

Naoto Fukuno, Hiroyuki Matsui, Osamu Suzuki, Keiichi Sasaki, Takayasu Kobayashi, Shinri Tamura

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

Mechanical stress plays an essential role in bone homeostasis by regulationg both bone formation and resorption. We have previously shown that cyclic stretch loading to MC3T3-E1 cells induced the expression of two bone remodeling related genes, Fn14 and MCP-3, through activation of ASK1 (a MAPKKK)/JNK and ASK1/p38 pathways, respectively. Here we show that cyclic stretch loading also induced the activation of TAK1 (another MAPKKK). Using TAK1 specific inhibitor 5Z-7 oxozeaenol, we revealed that TAK1 was required for the activation of at least four downstream pathways, namely, JNK, p38, NF-κB and NLK pathways. Moreover, TAK1 is activated via Ca2+-CaMKII pathway, resembling the non-canonical Wnt signaling pathway. These observations raise the possibility that TAK1 also plays various essential roles in mechanical stess-induced bone remodeling by activating diverse downstream pathways.

Original languageEnglish
Title of host publication20th Anniversary MHS 2009 and Micro-Nano Global COE - 2009 International Symposium on Micro-NanoMechatronics and Human Science
Pages383-384
Number of pages2
DOIs
Publication statusPublished - 2009 Dec 1
Event20th Anniversary MHS 2009 and Micro-Nano Global COE - 2009 International Symposium on Micro-NanoMechatronics and Human Science - Nagoya, Japan
Duration: 2009 Nov 82009 Nov 11

Publication series

Name20th Anniversary MHS 2009 and Micro-Nano Global COE - 2009 International Symposium on Micro-NanoMechatronics and Human Science

Other

Other20th Anniversary MHS 2009 and Micro-Nano Global COE - 2009 International Symposium on Micro-NanoMechatronics and Human Science
Country/TerritoryJapan
CityNagoya
Period09/11/809/11/11

ASJC Scopus subject areas

  • Computer Science(all)
  • Control and Systems Engineering
  • Electrical and Electronic Engineering

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