β1-Adrenergic receptor downregulates the expression of cyclooxygenase-2

Sivan Brender, Liza Barki-Harrington

Research output: Contribution to journalArticlepeer-review

Abstract

Cyclooxygenase-2 (COX-2) catalyzes the rate-limiting step in the generation of prostanoids, and is thus one of the key players in the inflammatory process. Contrary to the constitutively expressed isoform COX-1, the expression of COX-2 is rapidly and transiently upregulated following pathological stimuli but little is known about pathways that mediate its degradation. Here we show that co-expression of COX-2 together with the β1 adrenergic receptor (β1AR) specifically lowers the expression of COX-2 in a dose-dependent manner. We further find that stimulation of the receptor for prolonged periods of time does not reverse the β1AR-induced decrease in COX-2, suggesting that this effect does not occur via classical β1-mediated signaling pathways. Rather we find that the half-life of COX-2 is significantly decreased in the presence of β1AR and that inhibition of the proteasome reverses the effect of the receptor on COX-2. Together these findings ascribe a new role for β1AR in the downregulation of COX-2.

Original languageEnglish
Pages (from-to)319-321
Number of pages3
JournalBiochemical and Biophysical Research Communications
Volume451
Issue number2
DOIs
StatePublished - 22 Aug 2014

Bibliographical note

Funding Information:
We thank Dr. Sagie Schif-Zuck for her assistance and expertise in the flow cytometry analyses. This work was supported by the BSF (United States-Israel Binational Scientific Foundation), project number 2009246.

Keywords

  • Cyclooxygenase-2
  • Degradation

ASJC Scopus subject areas

  • Molecular Biology
  • Biophysics
  • Biochemistry
  • Cell Biology

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