Angiotensin II regulates human vascular smooth muscle α-actin gene expression

Nabil S. Andrawis, Earl H. Ruley, Darrell R. Abernethy

Research output: Contribution to journalArticlepeer-review

Abstract

Angiotensin II (AII) has been shown to induce vascular smooth muscle cell (VSMC) hypertrophy and increased expression of vascular cytoskeletal proteins. We have studied basal and All-induced expression of the chloramphenicol acetyl transferase (CAT) gene driven by three fragments of the human vascular smooth muscle (SM) α-actin promoter. We show basal CAT expression driven by the three fragments of the promoter when the constructs are transiently transfected into rat aortic VSMCs. All in a concentration-dependent manner (1.0 nM to 10 μM) increased expression of the CAT gene driven by 896 bp fragment. When comparing the 896 bp fragment to fragments successively deleted at the 5′ end (674 bp and 258 bp respectively), AII markedly stimulated CAT expression driven by the 896 bp fragment (257 ± 31% over control, p<0.01), stimulated CAT expression driven by 674 bp fragment to an apparently lesser degree (189 ± 20% over control, p<0.01), and tended to stimulate CAT expression driven by the 258 bp fragment, though not significantly greater than baseline (157 ± 28% of control). These data suggest that AII exerts transcriptional regulation of human SM α-actin gene through activation of cis-acting element(s) in an upstream area localized between positions -258 and -896 of the SM α-actin promoter. Such findings help establish the role of AII in enhancement of expression of components of the contractile apparatus.

Original languageEnglish (US)
Pages (from-to)962-968
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume196
Issue number2
DOIs
StatePublished - Oct 29 1993

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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