ET-1 Promotes Differentiation of Periodontal Ligament Stem Cells into Osteoblasts through ETR, MAPK, and Wnt/β-Catenin Signaling Pathways under Inflammatory Microenvironment

Mediators Inflamm. 2016:2016:8467849. doi: 10.1155/2016/8467849. Epub 2016 Jan 13.

Abstract

Periodontitis is a kind of chronic inflammatory disease that affects the tooth-supporting tissues. ET-1 is related to periodontitis and involved in the regulation of cytokines, but the mechanisms remain unclear. The aim of this study is to investigate how ET-1 affects proinflammatory cytokine expression and differentiation in human periodontal ligament stem cells (PDLSCs). PDLSCs were isolated from the periodontal ligament tissues of periodontitis patients and then treated with ET-1 (1, 10, or 100 nM) for 12 h, 24 h, or 72 h. The osteogenic potential of PDLSCs was tested using ALP staining. TNF-α, IL-1β, and IL-6 levels were evaluated by ELISA and western blot. Runx2, OCN, and COL1 mRNA and western levels were detected by RT-PCR and western blot, respectively. To examine the signaling pathways and molecular mechanisms involved in ET-1-mediated cytokine expression and osteogenic differentiation, ETR pathway, MAPKs pathway, Wnt/β-catenin pathway, and Wnt/Ca(2+) pathway were detected by RT-PCR and western blot, respectively. ET-1 promoted differentiation of PDLSCs into osteoblasts by increasing secretion of TNF-α, IL-1β, and IL-6 in a dose- and time-dependent manner. ET-1 also increased expression of Runx2, OCN, and COL1. ET-1 promotes differentiation of PDLSCs into osteoblasts through ETR, MAPK, and Wnt/β-catenin signaling pathways under inflammatory microenvironment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Differentiation / drug effects
  • Cells, Cultured
  • Endothelin-1 / pharmacology*
  • Humans
  • Interleukin-6 / metabolism
  • Osteoblasts / cytology*
  • Osteoblasts / drug effects
  • Osteogenesis / drug effects
  • Periodontal Ligament / cytology*
  • Stem Cells / cytology*
  • Stem Cells / drug effects
  • Tumor Necrosis Factor-alpha / metabolism
  • Wnt Proteins / metabolism*
  • Wnt Signaling Pathway
  • beta Catenin / metabolism*

Substances

  • Endothelin-1
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Wnt Proteins
  • beta Catenin