RhHMGB1 drives osteoblast migration in a TLR2/TLR4- and NF-κB-dependent manner. Issue 1 (19th February 2016)

• Record Type: Journal Article
• Authors: Li, Ming-Jing; Li, Fan; Xu, Jian; Liu, Yu-Dong; Hu, Tao; Chen, Jian-Ting
• Is Part Of: Bioscience reports. Volume 36:Issue 1(2016)
• Publication Date: 2016-02-19
• Subjects: migration -- osteoblast -- proliferation -- recombinant human high mobility group box 1 protein (rhHMGB1) -- siRNA -- skeletal development; Molecular biology -- Periodicals; Cytology -- Periodicals; 572.8
• DOI: 10.1042/BSR20150239
• Languages: English
• ISSNs: 0144-8463

Abstract

Abstract : In this paper, we reported that rhHMGB1 could significantly enhance the migration of osteoblast without causing cytotoxic effects through the activation of NF-κB via TLR2 or TLR4, indicating a significant functional role for HMGB1 in skeletal development and bone restoration. Abstract : Osteoblast migration is significant in skeletal development. Recently, high mobility group box 1 protein (HMGB1) has been shown to highly expressed in cartilage to regulate endochondral ossification. Nevertheless, whether HMGB1 can modulate osteoblast proliferation and migration is poorly understood, as well as the intracellular signalling pathways that are involved in this process. Herein, we examined the effects of recombinant human HMGB1 (rhHMGB1) on the proliferation and migration of rat osteoblasts and investigated whether Toll-like receptor 2 (TLR2)- and TLR4-dependent signalling pathways are involved in the regulation of intracellular signalling. A transwell chamber assay was used to evaluate the migration of osteoblasts and the MTT assay was used to assess osteoblast proliferation. rhHMGB1 could significantly promote the migration of osteoblasts without inhibiting their proliferation. Meanwhile, rhHMGB1 can increase the nuclear translocation of nuclear factor-kappa B (NF-κB) p65. Specific siRNA constructs that target TLR2 or TLR4 could markedly inhibit HMGB1-induced migration of osteoblasts and HMGB1-enhanced activation of NF-κB. Collectively, HMGB1 could significantly enhance the migration of osteoblasts in vitro, and TLR2/TLR4-dependent NF-κB pathways are involved in HMGB1-induced osteoblast migration.