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β1-Adrenergic receptor downregulates the expression of cyclooxygenase-2.

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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Brender S,Barki-Harrington L

doi

10.1016/j.bbrc.2014.07.123

subject

Has Abstract

pub_date

2014-08-22 00:00:00

pages

319-21

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(14)01373-4

journal_volume

451

pub_type

杂志文章

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