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2016 ; 7
(ä): 459
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15-Deoxy-?(12,14)-Prostaglandin J(2) Modifies Components of the Proteasome and
Inhibits Inflammatory Responses in Human Endothelial Cells
#MMPMID27833612
Marcone S
; Evans P
; Fitzgerald DJ
Front Immunol
2016[]; 7
(ä): 459
PMID27833612
show ga
15-Deoxy-?(12,14)-prostaglandin J(2) (15d-PGJ(2)) is an electrophilic lipid
mediator derived from PGD(2) with potent anti-inflammatory effects. These are
likely to be due to the covalent modification of cellular proteins, via a
reactive ?,?-unsaturated carbonyl group in its cyclopentenone ring. This study
was carried out to identify novel cellular target(s) for covalent modification by
15d-PGJ(2) and to investigate the anti-inflammatory effects of the prostaglandin
on endothelial cells (EC). The data presented here show that 15d-PGJ(2) modifies
and inhibits components of the proteasome and consequently inhibits the
activation of the NF-?B pathway in response to TNF-?. This, in turn, inhibits the
adhesion and migration of monocytes toward activated EC, by reducing the
expression of adhesion molecules and chemokines in the EC. The effects are
consistent with the covalent modification of 13 proteins in the 19S particle of
the proteasome identified by mass spectrometry and the suppression of proteasome
function, and were similar to the effects seen with a known proteasome inhibitor
(MG132). The ubiquitin-proteasome system has been implicated in the regulation of
several inflammatory processes and the observation that 15d-PGJ(2) profoundly
affects the proteasome functions in human EC suggests that 15d-PGJ(2) may
regulate the progression of inflammatory disorders such as atherosclerosis.
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