miR-16-5p and miR-145-5p trigger apoptosis in human gingival epithelial cells by down-regulating BACH2

Periodontitis is the second most common dental disease worldwide. TNF-α is up-regulated in periodontal disease and induces inflammation and cell apoptosis in gingival epithelial cells (GECs). miRNAs/mRNA axis play an important role in cell progression and inflammation. However, studies on the pathogenesis of periodontitisare still scarce, especially in the regulation mechanism of miRNAs.

The expression and protein level of miR-16-5p, miR-145-5p, BACH2, and caspase 3 were determined by quantitative real time PCR and western blot, respectively. Cell viability was measured by MTT assay. Cell apoptosis was detected by flow cytometry. Dual-luciferase assay was applied to verify miR-16-5p and miR-145-5p target to the 3'UTR of BACH2.

TNF-α induced miR-16-5p, miR-145-5p and caspase 3 expression, inhibited cell viability, promoted cell apoptosis in GECs. However, down-regulated miR-16-5p and miR-145-5p can restore the effects of TNF-α on GECs. In addition, dual-luciferase assay determined that BACH2 was a common target of miR-16-5p and miR-145-5p. Knockdown of BACH2 induced GECs apoptosis. Of note, cell apoptosis induced by miR-16-5p mimic, miR-145-5p mimic, and TNF-α was significantly reversed by up-regulating BACH2.

miR-16-5p and miR-145-5p mediate apoptosis induced by TNF-α in human gingival epithelial cells by targeting BACH2.