Compressive force-produced CCN2 induces osteocyte apoptosis through ERK1/2 pathway.

• Hoshi Kenji

• Kawaki Harumi

• Takahashi Itiro

• Takeshita Nobuo

• Seiryu Masahiro

• Sakhr Murshid

• Masuda Taisuke

• Anada Takahisa

• Kato Ryushi

• Kitaura Hideki

• Suzuki Osamu

Bibliographic Information

Other Title

• 圧縮力負荷に伴い骨細胞より産生されたCCN2はERK1/2経路を介しアポトーシスを誘導する。

Abstract

Osteocytes produce various factors in response to mechanical stimuli. One such factor, CCN2 is thought to play a significant role in osteocyte responses to mechanical stimuli, but its function in osteocytes is not well understood. We analyzed chick osteocyte response to compressive force focusing on apoptosis and CCN2 by using our original culture device that can apply quantitative mechanical stimuli. Compressive force increased CCN2 gene expression and protein production, and induced apoptosis in osteocytes. Application of exogenous CCN2 protein induced apoptosis, and a neutralizing CCN2 antibody blocked loading-induced apoptosis. We further examined how CCN2 induce apoptosis in loaded osteocytes. In loaded osteocytes, ERK1/2 was phosphorylated, and an ERK1/2 inhibitor blocked loading-induced apoptosis. Application of exogenous CCN2 protein caused ERK1/2 phosphorylation, and the neutralizing CCN2 antibody inhibited loading-induced ERK1/2 phosphorylation. These results demonstrated that enhanced production of CCN2 in osteocytes under compressive force loading induces apoptosis through ERK1/2 pathway.

Journal

• Transactions of Japanese Society for Medical and Biological Engineering

  Transactions of Japanese Society for Medical and Biological Engineering 52 (Supplement), O-237-O-238, 2014

  Japanese Society for Medical and Biological Engineering

Details

• CRID: 1390001205267540736
• NII Article ID: 130004695790
• DOI: 10.11239/jsmbe.52.o-237
• ISSN: 18814379
• ISSN: 1347443X
• Text Lang: ja
• Data Source:
  • JaLC
  • CiNii Articles
• Abstract License Flag: Disallowed