Temporal effects of 17β-estradiol on caveolin-1 mRNA and protein in bovine aortic endothelial cells

Muthuvel Jayachandran, Toshio Hayashi, Daigo Sumi, Akihisa Iguchi, Virginia M. Miller

Research output: Contribution to journalArticle

36 Scopus citations

Abstract

Endothelial nitric oxide synthase (eNOS) is regulated both by caveolin-1 and 17β-estradiol (E2). Temporal relationships between effects of estrogen on caveolin-1 and nitric oxide (NO) are not known. Therefore, this study was designed to determine whether estrogen regulates caveolin-1 and, if so, whether such regulation corresponds to changes in nitrite/nitrate (NOx) production. Bovine aortic endothelial cells (BAECs) were cultured in the absence and presence of 17β-estradiol or 17α-estradiol (10-8 and 10-10 M) for 12, 24, and 48 h. eNOS protein expression and NOx production increased significantly after 24 h but not after 12-h treatment with 17β- and not 17α-estradiol. Both mRNA and protein for caveolin-1 were increased significantly only after 48-h treatment with E2, but eNOS protein and NOx production were decreased compared with cells treated for 24 h. These increases in caveolin-1 were inhibited by the estrogen receptor antagonist ICI-182,780 (10-6 M). Results of this study suggest that E2 stimulates caveolin-1 transcription and translation through estrogen receptor-mediated mechanisms. The results further suggest that estrogen may indirectly regulate NOx through caveolin-1 expression, which inhibits eNOS catalytic activity.

Original languageEnglish (US)
Pages (from-to)H1327-H1333
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume281
Issue number3 50-3
DOIs
StatePublished - 2001

Keywords

  • Endothelial nitric oxide synthase
  • Estrogen receptor
  • Nitric oxide

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Fingerprint Dive into the research topics of 'Temporal effects of 17β-estradiol on caveolin-1 mRNA and protein in bovine aortic endothelial cells'. Together they form a unique fingerprint.

  • Cite this