%0 Journal Article
%T microRNA-142 is upregulated by tumor necrosis factor-alpha and triggers apoptosis in human gingival epithelial cells by repressing BACH2 expression
%A Jiachen Dong
%A Rong Shu
%A Song Li
%A Zhongchen Song
%J Archive of "American Journal of Translational Research".
%D 2017
%X Tumor necrosis factor-alpha (TNF-¦Á) has been shown to cause apoptosis of gingival epithelial cells (GECs) in periodontitis. However, the underlying molecular mechanism is still unclear. In this study, we showed that miR-142 expression was significantly elevated in human GECs after exposure to TNF-¦Á. Such induction was in a time- and concentration-dependent manner. Serum miR-142 levels were positively correlated with serum TNF-¦Á levels in patients with chronic periodontitis (r = 0.314, P = 0.0152). Depletion of miR-142 was found to attenuate TNF-¦Á-induced apoptosis, as determined by TUNEL staining and caspase-3 activity assays. In contrast, overexpression of miR-142 significantly reduced viability and induced apoptosis in GECs. Basic leucine zipper transcription factor 2 (BACH2) was identified to be a functional target of miR-142. Overexpression of miR-142 caused a 3-fold reduction of BACH2 protein in primary GECs. Overexpression of BACH2 significantly reversed miR-142- or TNF-¦Á-induced apoptosis of GECs. Similar to the findings with miR-142 mimic, depletion of BACH2 significantly promoted apoptosis in GECs, which was accompanied by decreased expression of Bcl-2 and Bcl-xL and increased expression of Bax and Bim. Overall, miR-142 mediates TNF-¦Á-induced apoptosis in gingival epithelial cells by targeting BACH2 and may represent a potential therapeutic target for periodontitis
%K Apoptosis
%K chronic periodontitis
%K gingival epithelial cells
%K inflammatory cytokines
%K microRNA
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5250714/