title: [MiR-142-3p inhibits lipopolysaccharide-induced inflammatory response in human periodontal ligament cells through targeting IRAK1].
abstract: OBJECTIVE
  To investigate the effects of miR-142-3p overexpression on secretion of inflammatory factors in human periodontal ligament cells (hPDLCs) induced by lipopolysaccharide (LPS) and its underlying mechanism.
  
  
  METHODS
  hPDLCs were cultured by tissue cultivation in vitro and treated with various concentrations of LPS for 6, 12, 24 and 48 h. hPDLCs were treated with miR-142-3p mimics for 24 h in the presence of 2.0 μg/mL LPS and the expression levels of inflammatory factors (TNF-α, IL-6 and IL-1β) were detected by ELISA assay. The target relationship between miR-142-3p and interleukin-1 receptor- associated kinase 1 (IRAK1) was detected by dual-luciferase reporter assay. The miR-142-3p and IRAK1 mRNA expression was measured by qRT-PCR. The protein expression levels of IRAK1, TLR4 and NF-κB were detected by Western blotting. Statistical analysis was performed using SPSS 16.0 software package.
  
  
  RESULTS
  The miR-142-3p expression level was decreased significantly at 24 h in 2.0 μg/mL LPS-treated hPDLCs (P<0.01). Transfection of miR-142-3p mimics remarkably increased miR-142-3p expression (P<0.01). The secretion of inflammatory factors (TNF-α, IL-6 and IL-1β) in LPS-treated hPDLCs was significantly decreased by miR-142-3p overexpression (P<0.05). Dual-luciferase reporter assay showed a directly targeting relationship between miR-142-3p and IRAK1. Overexpression of miR-142-3p significantly reduced the IRAK1 protein expression in LPS-treated hPDLCs (P<0.05), whereas no obvious effect on IRAK1 mRNA expression was noted (P>0.05). Moreover, miR-142-3p overexpression markedly diminished the protein expression of TLR4 and phosphorylated NF-κB in LPS-treated hPDLCs (P<0.05).
  
  
  CONCLUSIONS
  Overexpression of miR-142-3p can alleviate the inflammatory response induced by LPS in hPDLCs and the underlying mechanism may be associated with targeting and inhibiting IRAK1 expression leading to suppression of TLR4/NF-κB inflammatory signaling pathway through which miR-142-3p overexpression protects peridentium against inflammation.
authors.affiliation: Department of Prosthodontics, Yanan Affiliated Hospital of Yanan University. Yanan 716000, Shaanxi Province, China. E-mail:hbo_liu@126.com.
authors.forename: Hai-Yan
authors.initials: HY
authors.lastname: Hu
authors.forename: Jun-Qiang
authors.initials: JQ
authors.lastname: Wang
mesh_terms: D002460:Cell Line; D006801:Humans; D007249:Inflammation; D053592:Interleukin-1 Receptor-Associated Kinases / Q000378:metabolism*; D015850:Interleukin-6; D008070:Lipopolysaccharides / Q000378:metabolism*; D035683:MicroRNAs; D016328:NF-kappa B; D010513:Periodontal Ligament / Q000502:physiology*; D015398:Signal Transduction; D014162:Transfection; D014409:Tumor Necrosis Factor-alpha
chemical_list: D015850:Interleukin-6; D008070:Lipopolysaccharides; D035683:MicroRNAs; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D053592:Interleukin-1 Receptor-Associated Kinases