Cyclic stretch induces cyclooxygenase-2 gene expression in vascular endothelial cells via activation of nuclear factor kappa-β

Haige Zhao, Toyoko Hiroi, Baranda S. Hansen, Jeffrey J. Rade

Research output: Contribution to journalArticle

Abstract

Vascular endothelial cells respond to biomechanical forces, such as cyclic stretch and shear stress, by altering gene expression. Since endothelial-derived prostanoids, such as prostacyclin and thromboxane A2, are key mediators of endothelial function, we investigated the effects of cyclic stretch on the expression of genes in human umbilical vein endothelial cells controlling prostanoid synthesis: cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), prostacyclin synthase (PGIS) and thromboxane A2 synthase (TXAS). COX-2 and TXAS mRNAs were upregulated by cyclic stretch for 24 h. In contrast, PGIS mRNA was decreased and stretch had no effect on COX-1 mRNA expression. We further show that stretch-induced upregulation of COX-2 is mediated by activation of the NF-κβ signaling pathway.

Original languageEnglish (US)
Pages (from-to)599-601
Number of pages3
JournalBiochemical and Biophysical Research Communications
Volume389
Issue number4
DOIs
StatePublished - Nov 27 2009

Fingerprint

Thromboxane A2
Endothelial cells
Cyclooxygenase 2
Gene expression
Cyclooxygenase 1
Endothelial Cells
Chemical activation
Gene Expression
Messenger RNA
Prostaglandins
Human Umbilical Vein Endothelial Cells
Epoprostenol
Shear stress
Up-Regulation
Genes

Keywords

  • COX-1
  • COX-2
  • Cyclic stretch
  • Endothelial cells
  • Nuclear factor kappa-β
  • Prostacyclin synthase
  • Thromboxane synthase

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Molecular Biology

Cite this

Cyclic stretch induces cyclooxygenase-2 gene expression in vascular endothelial cells via activation of nuclear factor kappa-β. / Zhao, Haige; Hiroi, Toyoko; Hansen, Baranda S.; Rade, Jeffrey J.

In: Biochemical and Biophysical Research Communications, Vol. 389, No. 4, 27.11.2009, p. 599-601.

Research output: Contribution to journalArticle

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