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Hyaluronic acid (HA) is a widely distributed component of the extracellular matrix that has been shown to play regulatory roles in inflammation. In the present study, we examined the inhibitory mechanism of HA related to mechanical stress-induced inflammatory response in mouse gingival epithelial GE1 cells. Application of compressive force in a three-dimensional cell culture system increased the expression of cyclooxygenase-2 (COX-2) mRNA in a force-dependent manner, while COX-2 protein and prostaglandin E2 (PGE2) levels were also increased in a time-dependent manner. Interestingly, we found that HA suppressed the expression of COX-2 and production of PGE2 under the same conditions. Western blotting analysis revealed that mechanical stress induced the phosphorylation of ERK and p38 MAPK at 60 minutes after loading, while that of IκBα was activated at 15 minutes and peaked at 30 minutes. In addition, IκBα degradation was activated at 30 minutes and recovered at 60 minutes. Furthermore, treatment with HA down-regulated the phosphorylation of p38 MAPK, ERK, and IκBα in GE1 cells. These results indicate that mechanical stress enhances the induction of COX-2 and PGE2 in epithelial cells, while HA inhibits those mechanical stress-induced inflammatory responses via MAPKs and the NF-κB signaling pathway.

Inflammatory response in epithelial cells induced by mechanical stress is suppressed by hyaluronic acid