The histone deasetylase HDAC1 expression in human periodontitis – preliminary results

ORCiD

Ana C. Morandini: 0000-0003-4749-571X

Department

Biomedical Sciences

Document Type

Conference Presentation

Conference Title

4th European Congress of Immunology

Location

Vienna, Austria

Conference Dates

September 6-9, 2015

Date of Presentation

1-1-2015

Abstract

Introduction: Fibroblasts are now seen as active components of the immune response because these cells are able to mediate the production of cytokines during inflammation. Among the molecular mechanisms that can regulate gene expression are epigenetic processes, which can be mediated by histone deacetylases (HDACs). However, little is known about the specific role of HDAC1 in the regulation of inflammatory response by gingival fibroblasts and in periodontal infection. Here, we investigated the expression profile of HDAC1 in patients with and without chronic periodontitis, as well as the impact of conventional periodontal treatment in HDAC1 expression. We also explored HDAC1 expression in human gingival fibroblasts (HGF) infected with Porphyromonas gingivalis, a well-known periodontopathogen.

Material and Methods: Primary HGF from healthy donors were challenged with P. gingivalis for 6 h or 24 h and subsequently evaluated for HDAC1 mRNA (RT-qPCR) and protein expression (Western blot and immunofluorescence). Also, human gingival tissues from periodontitis patients before and after conventional periodontal treatment were compared regarding HDAC1 mRNA.

Results: We found lower levels of HDAC1 in chronic periodontitis patients when compared with controls, which were maintained after conventional periodontal treatment. P.gingivalisinfection increased HDAC1 protein expression after 6 h, which was decreased after 24 h. Immunofluorescence staining also revealed HDAC1 reduction during P. gingivalis infection.

Conclusion: These findings are consistent with a potential role for epigenetic regulation of HDAC1 in human periodontal disease. Also, P. gingivalis was able to downregulate HDAC1 in HGF. Ongoing studies will better clarify the role of HDAC1 in P.gingivalis infection.

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