Ets-1 regulates TNF-alpha-induced matrix metalloproteinase-9 and tenascin expression in primary bronchial fibroblasts

J Immunol. 2004 Feb 1;172(3):1945-52. doi: 10.4049/jimmunol.172.3.1945.

Abstract

Increased subepithelial deposition of extracellular matrix proteins is a key feature in bronchial asthma. Matrix metalloproteinase-9 (MMP-9) is a proteolytic enzyme that degrades the extracellular matrix. Tenascin is an extracellular matrix glycoprotein that is abundant in thickened asthmatic subbasement membrane. The expression of MMP-9 and tenascin reflects disease activity in asthma and airway remodeling. The molecular mechanisms regulating the expression of these proteins remain unknown. Both MMP-9 and tenascin promoters contain an Ets binding site, suggesting control by Ets-1. Thus, we hypothesized that Ets-1 expression is increased in asthma and that it contributed to enhanced MMP-9 and tenascin expression. To test this hypothesis, we determined the expression of Ets-1 in bronchial biopsies obtained from asthmatic subjects and determined the expression of Ets-1, MMP-9, and tenascin by bronchial fibroblasts activated ex vivo. We observed that nuclear extracts from TNF-alpha-activated fibroblasts showed increased Ets-binding activity. In addition, TNF-alpha-activated fibroblasts had increased expression of Ets-1 mRNA and protein, which preceded an increase in MMP-9 and tenascin mRNA. Furthermore, treatment of fibroblasts with Ets-1 antisense oligonucleotides down-regulated TNF-alpha-induced Ets-1, MMP-9, and, to a lesser extent, tenascin protein expression or activity. Taken together, these data demonstrate that TNF-alpha increases MMP-9 and tenascin expression in bronchial fibroblasts via the transcription factor Ets-1, and suggest a role for Ets-1 in airway remodeling in asthma.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Asthma / enzymology
  • Asthma / immunology
  • Asthma / metabolism*
  • Bronchi / cytology
  • Bronchi / enzymology
  • Bronchi / immunology
  • Bronchi / metabolism*
  • Cells, Cultured
  • DNA-Binding Proteins / antagonists & inhibitors
  • DNA-Binding Proteins / metabolism
  • Enzyme Induction / immunology
  • Female
  • Fibroblasts / enzymology
  • Fibroblasts / immunology*
  • Fibroblasts / metabolism*
  • Fluorescein-5-isothiocyanate / metabolism
  • Humans
  • Male
  • Matrix Metalloproteinase 9 / biosynthesis*
  • Matrix Metalloproteinase 9 / genetics
  • Oligonucleotides, Antisense / genetics
  • Oligonucleotides, Antisense / metabolism
  • Oligonucleotides, Antisense / pharmacology
  • Protein Binding / immunology
  • Proto-Oncogene Protein c-ets-1
  • Proto-Oncogene Proteins / biosynthesis
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins / physiology*
  • Proto-Oncogene Proteins c-ets
  • RNA, Messenger / biosynthesis
  • Respiratory Mucosa / metabolism
  • Tenascin / biosynthesis*
  • Tenascin / genetics
  • Thionucleotides / genetics
  • Thionucleotides / metabolism
  • Transcription Factors / biosynthesis
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Transcription Factors / physiology*
  • Transfection
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Up-Regulation / physiology

Substances

  • DNA-Binding Proteins
  • ETS1 protein, human
  • Oligonucleotides, Antisense
  • Proto-Oncogene Protein c-ets-1
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-ets
  • RNA, Messenger
  • Tenascin
  • Thionucleotides
  • Transcription Factors
  • Tumor Necrosis Factor-alpha
  • Matrix Metalloproteinase 9
  • Fluorescein-5-isothiocyanate