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Short Communication |
(PPAR) Expression and Reduction of MMP-9 Activitythrough PPAR Activation in Mononuclear Phagocytes inVitro
From the Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
Mononuclear phagocytes play an important role in atherosclerosis
and its sequela plaque rupture in part by their secretion of matrix
metalloproteinases (MMPs), including MMP-9. Peroxisomal
proliferator-activated receptor 
(PPAR), a transcription
factor in the nuclear receptor superfamily, regulates gene
expression in response to various activators, including
15-deoxy-
12,14-prostaglandin J2 and
the antidiabetic agent troglitazone. The role of PPAR in human
atherosclerosis is unexplored. We report here that
monocytes/macrophages in human atherosclerotic lesions
(n = 12) express immunostainable PPAR. Normal
artery specimens (n = 6) reveal minimal
immunoreactive PPAR. Human monocytes and monocyte-derived
macrophages cultured for 6 days in 5% human serum expressed PPAR
mRNA and protein by reverse transcription-polymerase chain reaction and
Western blotting, respectively. In addition, PPAR
mRNA expression in U937 cells increased during phorbol 12-myristate 13
acetate-induced differentiation. Stimulation of PPAR with
troglitazone or 15-deoxy-12,14-prostaglandin
J2 in human monocyte-derived macrophages inhibited MMP-9
gelatinolytic activity in a concentration-dependent fashion as revealed
by zymography. This inhibition correlates with decreased MMP-9
secretion as determined by Western blotting. Thus, PPAR is
present in macrophages in human atherosclerotic lesions and may
regulate expression and activity of MMP-9, an enzyme implicated
in plaque rupture. PPAR is likely to be an important regulator of
monocyte/macrophage function with relevance for human atherosclerotic
disease.
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