Histone acetylation is involved in LPS-induced inflammation in DPCs

Objectives: Pulpitis is a common inflammatory disease in dental clinic. However, to date, given that the mechanism regarding responses to inflammatory stimuli remains largely unknown, scientists and dentists do not find a good way to rescue the inflammatory dental pulp and turn the destination of pulp cells to restore/regenerate dental pulp tissue as well as dentin. The aim of this study was to investigate whether histone acetylation is involved in the process of LPS-induced inflammation in dental pulp cells (DPCs).
Methods: DPCs were cultures from healthy donors, and the 4-6^th passages cells were used to do the following assays. DPCs were stimulated with LPS for 3 h, then the proteins were harvested for detecting the expression of acetylation by using anti-pan-acetyllysine antibody. Co-IP combined with mass spectrometry was applied to find the differential expression acetylated proteins. Histone deacetylase inhibitor sodium butyrate was applied to treat DPCs instead of LPS, to reconfirm that acetylation is involved in the LPS-induced inflammation in dental pulp cells (DPCs). Acetylase inhibitor (curcumin) was used to block the process of LPS-induced acetylation, and then detect the expression of inflammatory mediators including IL-β, IL-1RA, IL-6, IL-8 , IL-10 and TNF-α by cytokine array and real-time PCR, and detect inflammation-related pathway proteins expression.
Results: Western blot showed that acetylation was involved in the process of LPS-induced inflammation in DPCs. Co-IP combined with mass spectrometry results showed some proteins including histone acetylation. Histone deacetylase inhibitor sodium butyrate has a potential to induce the release of inflammatory mediators. After applied by curcumin, LPS-induced inflammatory mediator expression pattern was changed accordingly.
Conclusions: Histone acetylation plays an important role in the process of LPS-induced inflammatory response probably through acetylation of the potential targets, which indicates alteration of acetylation of DPCs may change inflammatory reactions and affect the destination of DPCs’fate in future.