HtrA1 is upregulated during RANKL-induced osteoclastogenesis, and negatively regulates osteoblast differentiation and BMP2-induced Smad1/5/8, ERK and p38 phosphorylation

X. Wu, Shek Chim, V. Kuek, B.S. Lim, Siu To Chow, J. Zhao, S. Yang, V. Rosen, Jennifer Tickner, Jiake Xu

Research output: Contribution to journalArticlepeer-review

29 Citations (Scopus)

Abstract

Bone remodeling is regulated by secreted factors in the bone microenvironment. However, data regarding osteoclast-derived factors that influence osteoblast differentiation are lacking. Here, we show that HtrA1 is produced as a secreted protein during osteoclastogenesis, and negatively regulates osteoblast differentiation. Exogenous addition of recombinant HtrA1 attenuates osteoblast differentiation and BMP2-induced Smad1/5/8, ERK1/2 and p38 phosphorylation in pre-osteoblasts. Our studies imply a unique mode of crosstalk in which HtrA1 is produced by both osteoclasts and osteoblasts and negatively regulates osteoblast differentiation, suggesting that HtrA1 may mediate the fine tuning of paracrine and autocrine regulations during bone remodeling processes.
Original languageEnglish
Pages (from-to)143-150
JournalFEBS Letters
Volume588
Issue number1
Early online date21 Nov 2013
DOIs
Publication statusPublished - Jan 2014

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