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BMB Rep. 2017 Feb;50(2):97-102.

Extracellular S100A4 negatively regulates osteoblast function by activating the NF-κB pathway.

Author information

1
Department of Cell and Developmental Biology, BK21 Program and DRI, School of Dentistry, Seoul National University, Seoul 03080, Korea.

Abstract

Patients with inflammatory bone disease or cancer exhibit an increased risk of fractures and delayed bone healing. The S100A4 protein is a member of the calcium-binding S100 protein family, which is abundantly expressed in inflammatory diseases and cancers. We investigated the effects of extracellular S100A4 on osteoblasts, which are cells responsible for bone formation. Treating primary calvarial osteoblasts with recombinant S100A4 resulted in matrix mineralization reductions. The expression of osteoblast marker genes including osteocalcin and osterix was also suppressed. Interestingly, S100A4 stimulated the nuclear factor-kappaB (NF-κB) signaling pathway in osteoblasts. More importantly, the ex vivo organ culture of mouse calvariae with recombinant S100A4 decreased the expression levels of osteocalcin, supporting the results of our in vitro experiments. This suggests that extracellular S100A4 is important for the regulation of bone formation by activating the NF-κB signaling pathway in osteoblasts. [BMB Reports 2017; 50(2): 97-102].

PMID:
27998393
PMCID:
PMC5342873
DOI:
10.5483/bmbrep.2017.50.2.170
[Indexed for MEDLINE]
Free PMC Article

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