GATA6 inhibits the periodontitis progression through regulating the Notch signaling pathway.

Abstract

Periodontitis is a prevalent chronic infectious condition affecting the oral cavity. This research was conducted to analyze the role of GATA6 in LPS-stimulated human periodontal ligament cells (hPDLCs). Dysregulated genes associated with periodontitis were acquired from the GEO database (GSE23586). Cell viability was measured utilizing the MTT assay, while apoptosis was analyzed through flow cytometry. The expression levels of mRNA and proteins were examined using qRT-PCR and Western blot techniques, respectively. Levels of IL-1β, IL-6, and TNF-α were measured using specific ELISA kits. The mouse periodontitis model was established to evaluate the effect of GATA transcription factor 6 (GATA6) in vivo.The results demonstrated that GATA6 was downregulated in periodontitis and LPS-stimulated hPDLCs. Overexpression of GATA6 enhanced cell viability, while inhibited apoptosis in hPDLCs. It also reduced the levels of IL-1β, IL-6, and TNF-α in LPS-stimulated hPDLCs. Additionally, after transfection with a GATA6 overexpression vector, the expressions of Caspase 3 and Bax proteins were suppressed, while Bcl2 was upregulated. Furthermore, in LPS-stimulated hPDLCs, the protein levels of Notch1, Hey1, and Hey2 were enhanced after GATA6 overexpression. Silencing of Notch1 neutralized the effects of GATA6 in LPS-stimulated hPDLCs. In addition, GATA6 overexpression alleviated the progression of periodontitis in vivo. In conclusion, GATA6 alleviated the progression of periodontitis by activating the Notch signaling pathway.