PMID- 28123644
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1943-8141 (Print)
IS  - 1943-8141 (Electronic)
IS  - 1943-8141 (Linking)
VI  - 9
IP  - 1
DP  - 2017
TI  - microRNA-142 is upregulated by tumor necrosis factor-alpha and triggers apoptosis 
      in human gingival epithelial cells by repressing BACH2 expression.
PG  - 175-183
AB  - Tumor necrosis factor-alpha (TNF-alpha) 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-alpha. Such induction was 
      in a time- and concentration-dependent manner. Serum miR-142 levels were 
      positively correlated with serum TNF-alpha levels in patients with chronic 
      periodontitis (r = 0.314, P = 0.0152). Depletion of miR-142 was found to 
      attenuate TNF-alpha-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-alpha-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-alpha-induced apoptosis in gingival epithelial cells by 
      targeting BACH2 and may represent a potential therapeutic target for 
      periodontitis.
FAU - Li, Song
AU  - Li S
AD  - Department of Periodontology, Ninth People's Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai Key Laboratory of Stomatology & Shanghai 
      Research Institute of StomatologyShanghai, China; Jiangsu Key Laboratory of Oral 
      Diseases, Department of Periodontology, Affiliated Hospital of Stomatology, 
      Nanjing Medical UniversityNanjing, China.
FAU - Song, Zhongchen
AU  - Song Z
AD  - Department of Periodontology, Ninth People's Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai Key Laboratory of Stomatology & Shanghai 
      Research Institute of Stomatology Shanghai, China.
FAU - Dong, Jiachen
AU  - Dong J
AD  - Department of Periodontology, Ninth People's Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai Key Laboratory of Stomatology & Shanghai 
      Research Institute of Stomatology Shanghai, China.
FAU - Shu, Rong
AU  - Shu R
AD  - Department of Periodontology, Ninth People's Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai Key Laboratory of Stomatology & Shanghai 
      Research Institute of Stomatology Shanghai, China.
LA  - eng
PT  - Journal Article
DEP - 20170115
PL  - United States
TA  - Am J Transl Res
JT  - American journal of translational research
JID - 101493030
PMC - PMC5250714
OTO - NOTNLM
OT  - Apoptosis
OT  - chronic periodontitis
OT  - gingival epithelial cells
OT  - inflammatory cytokines
OT  - microRNA
EDAT- 2017/01/27 06:00
MHDA- 2017/01/27 06:01
PMCR- 2017/01/15
CRDT- 2017/01/27 06:00
PHST- 2016/07/07 00:00 [received]
PHST- 2016/12/29 00:00 [accepted]
PHST- 2017/01/27 06:00 [entrez]
PHST- 2017/01/27 06:00 [pubmed]
PHST- 2017/01/27 06:01 [medline]
PHST- 2017/01/15 00:00 [pmc-release]
PST - epublish
SO  - Am J Transl Res. 2017 Jan 15;9(1):175-183. eCollection 2017.