Regulation of hypoxia-inducible factor-1α in human buccal mucosal fibroblasts stimulated with arecoline

J Formos Med Assoc. 2017 Jun;116(6):484-487. doi: 10.1016/j.jfma.2017.02.019. Epub 2017 Mar 30.

Abstract

Hypoxia-inducible factor (HIF)-1α is consistently and dramatically upregulated in a variety of fibrotic diseases. The aim of this study was to compare HIF-1α expression from fibroblasts derived from human normal buccal mucosa and oral submucous fibrosis (OSF) specimens and further to explore the potential mechanisms that may lead to induce HIF-1α expression. OSF buccal mucosal fibroblasts (BMFs) demonstrated significantly higher HIF-1α mRNA expression than normal BMFs (p<0.005). Arecoline, the major areca nut alkaloid, was also found to elevate HIF-1α mRNA expression in a dose-dependent manner (p<0.05). Moreover, arecoline-induced HIF-1α expression was downregulated by mitogen-activated protein kinase inhibitor U0126, phosphatidylinositol 3-kinase inhibitor LY294002, p38 inhibitor SB203580, cyclooxygenase-2 inhibitor NS-398, and glutathione precursor N-acetyl-L-cysteine (p<0.05). Taken together, hypoxia plays an important role in the pathogenesis of areca quid chewing-associated OSF. These pharmacological agents may be further used as chemoprevention agents for OSF.

Keywords: arecoline; hypoxia-inducible factor; oral submucous fibrosis; regulatory mechanisms.

MeSH terms

  • Arecoline / pharmacology*
  • Case-Control Studies
  • Cholinergic Agonists / pharmacology*
  • Fibroblasts / metabolism*
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / drug effects*
  • Hypoxia-Inducible Factor 1, alpha Subunit / genetics
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism*
  • Mouth Mucosa / metabolism*
  • Oral Submucous Fibrosis / metabolism
  • RNA, Messenger / metabolism

Substances

  • Cholinergic Agonists
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • RNA, Messenger
  • Arecoline