Expression of high mobility group box 1 in inflamed dental pulp and its chemotactic effect on dental pulp cells
•HMGB1 translocated from nucleus to cytoplasm during dental pulp inflammation.•HMGB1and its receptor RAGE were up-regulated in hDPCs under LPS stimulation.•HMGB1 enhanced hDPCs migration and induces cytoskeleton reorganization.•HMGB1 may play a critical role in dental pulp repair during inflamed sta...
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Veröffentlicht in: | Biochemical and biophysical research communications 2014-08, Vol.450 (4), p.1547-1552 |
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Sprache: | eng |
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Zusammenfassung: | •HMGB1 translocated from nucleus to cytoplasm during dental pulp inflammation.•HMGB1and its receptor RAGE were up-regulated in hDPCs under LPS stimulation.•HMGB1 enhanced hDPCs migration and induces cytoskeleton reorganization.•HMGB1 may play a critical role in dental pulp repair during inflamed state.
High mobility group box 1 protein (HMGB1) is a chromatin protein which can be released extracellularly, eliciting a pro-inflammatory response and promoting tissue repair process. This study aimed to examine the expression and distribution of HMGB1 and its receptor RAGE in inflamed dental pulp tissues, and to assess its effects on proliferation, migration and cytoskeleton of cultured human dental pulp cells (DPCs). Our data demonstrated that cytoplasmic expression of HMGB1 was observed in inflamed pulp tissues, while HMGB1 expression was confined in the nuclei in healthy dental pulp. The mRNA expression of HMGB1 and RAGE were significantly increased in inflamed pulps. In in vitro cultured DPCs, expression of HMGB1 in both protein and mRNA level was up-regulated after treated with lipopolysaccharide (LPS). Exogenous HMGB1 enhanced DPCs migration in a dose-dependent manner and induced the reorganization of f-actin in DPCs. Our results suggests that HMGB1 are not only involved in the process of dental pulp inflammation, but also play an important role in the recruitment of dental pulp stem cells, promoting pulp repair and regeneration. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2014.07.027 |