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IL-17 inhibits osteoblast differentiation and bone regeneration in rat

Authors :
Yong-Gun Kim
Beom-Seok Chang
Heung-Sik Um
Jae-Mok Lee
Jo-Young Suh
Youngkyun Lee
Jae-Young Kim
Jae-Kwan Lee
Jin-Woo Park
Source :
Archives of Oral Biology. 59:897-905
Publication Year :
2014
Publisher :
Elsevier BV, 2014.

Abstract

Objective The interleukin-17 (IL-17) family is a group of pro-inflammatory cytokines that are produced by a subset of helper T cells. IL-17 family members are not only involved in the immune response of tissues but also play a role in bone metabolism. Although the role of IL-17 in osteoclast-mediated bone resorption has been extensively studied, its role during osteoblast-mediated bone formation has rarely been investigated. In this study, we examined the effect of IL-17 on osteogenesis in rats both in vitro and in vivo . Design To evaluate osteogenesis in vitro , rat calvarial osteoblast precursor cells were cultured for 14 days in osteogenic medium with or without 50ng/mL IL-17. Osteogenic activity was evaluated by alkaline phosphatase and alizarin red staining. The mRNA expression of alkaline phosphatase, osteocalcin, and osterix was also measured by using real-time PCR. To test whether IL-17 affects bone formation in vivo , bone filling was examined by micro-computed tomography and histological observations at 8 weeks after critical-sized defects were made in rat calvaria. Results The presence of IL-17 significantly reduced alkaline phosphatase and alizarin red staining and the expression of alkaline phosphatase, osteocalcin, and osterix in vitro . IL-17 also significantly inhibited the filling of calvarial defects in vivo . Conclusion IL-17 exerted a negative effect on osteogenesis in a rat model. In contrast to the previously reported beneficial effect on osteogenic differentiation of human mesenchymal stem cells, our results suggest a species or cell type-specific role for IL-17 in bone formation.

Details

ISSN :
00039969
Volume :
59
Database :
OpenAIRE
Journal :
Archives of Oral Biology
Accession number :
edsair.doi.dedup.....5acabbb2c53821ba429754295484b522