Ets-1 is an early response gene activated by ET-1 and PDGF-BB in vascular smooth muscle cells

Am J Physiol. 1998 Feb;274(2):C472-80. doi: 10.1152/ajpcell.1998.274.2.C472.

Abstract

Ets-1 is a transcription factor that activates expression of matrix-degrading proteinases such as collagenase and stromelysin. To study the control of ets-1 gene expression in rat vascular smooth muscle cells (VSMC), cells were exposed to factors known to regulate VSMC migration and proliferation. Platelet-derived growth factor-BB (PDGF-BB), endothelin-1 (ET-1), and phorbol 12-myristate 13-acetate (PMA) induced a dose-dependent expression of ets-1 mRNA. These effects were abrogated by inhibition of protein kinase C (PKC) by H-7 or chronic PMA treatment. Ets-1 mRNA was superinduced by PDGF-BB and ET-1 in the presence of cycloheximide. The chelation of intracellular Ca2+ by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester and the depletion of endoplasmic reticulum intracellular Ca2+ concentration ([Ca2+]i) by thapsigargin inhibited PDGF-BB- and ET-1-induced ets-1 mRNA, whereas ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid had no effect. However, [Ca2+]i release alone was not sufficient to increase ets-1 mRNA. Forskolin blocked ET-1-, PDGF-BB-, and PMA-induced ets-1 mRNA, as well as inositol phosphate formation, consistent with an effect through impairment of PKC activation. Inhibitors of ets-1 gene expression, such as H-7 and herbimycin A, inhibited the ET-1 induction of collagenase I mRNA. We propose that ets-1 may be an important element in the orchestration of matrix proteinase expression and of vascular remodeling after arterial injury.

Publication types

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

MeSH terms

  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / pharmacology
  • Animals
  • Becaplermin
  • Benzoquinones
  • Calcium / metabolism
  • Cells, Cultured
  • Collagenases / genetics
  • Collagenases / metabolism
  • Culture Media, Serum-Free
  • Cyclic AMP / pharmacology
  • Cycloheximide / pharmacology
  • Endoplasmic Reticulum / metabolism
  • Endothelin-1 / pharmacology*
  • Enzyme Activation
  • Enzyme Inhibitors / pharmacology
  • Extracellular Matrix / metabolism
  • Gene Expression Regulation / drug effects*
  • Lactams, Macrocyclic
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / metabolism*
  • Platelet-Derived Growth Factor / pharmacology*
  • Protein Kinase C / metabolism
  • Protein Synthesis Inhibitors / pharmacology
  • Proto-Oncogene Protein c-ets-1
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins c-ets
  • Proto-Oncogene Proteins c-sis
  • Quinones / pharmacology
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Rifabutin / analogs & derivatives
  • Transcription Factors / genetics*
  • Transcription, Genetic / drug effects

Substances

  • Benzoquinones
  • Culture Media, Serum-Free
  • Endothelin-1
  • Enzyme Inhibitors
  • Ets1 protein, rat
  • Lactams, Macrocyclic
  • Platelet-Derived Growth Factor
  • Protein Synthesis Inhibitors
  • Proto-Oncogene Protein c-ets-1
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-ets
  • Proto-Oncogene Proteins c-sis
  • Quinones
  • RNA, Messenger
  • Transcription Factors
  • Becaplermin
  • Rifabutin
  • herbimycin
  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • Cycloheximide
  • Cyclic AMP
  • Protein Kinase C
  • Collagenases
  • Calcium