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(Circulation. 2003;108:e9016.)
© 2003 American Heart Association, Inc.

Cardiovascular News

Ruth SoRelle, MPH

Circulation Newswriter

An extract of the first 250 words of the full text is provided, because this article has no abstract.

RAGE May Influence Diabetic Plaque Rupture

RAGE—the receptor for advanced glycation end products—may enhance the inflammatory reaction and expression of cyclooxygenase-2 and prostaglandin E (PGE) synthase-1 (COX-2/mPGES-1) in patients with diabetes, thus advancing the cascade of events that can lead to plaque rupture within human arteries, said Italian and US researchers in this week’s issue of the journal Circulation (Circulation. 2003;108:1070–1077)[Abstract/Free Full Text].

The researchers, led by Francesco Cipollone, MD, of the University of Chieti "G D’Annunzio" School of Medicine, had already provided evidence that COX-2/mPGES-1 was associated with metalloproteinase-induced plaque rupture. In an attempt to identify the transmembrane signaling pathways influencing the expression of COX-2/mPGES-1, they sought to characterize RAGE expression in human plaque. Plaques from the carotid arteries of 60 patients who had undergone endarterectomy were divided into diabetic and nondiabetic categories. The plaques were then analyzed to determine RAGE, nuclear factor (NF)-B, COX-2/mPGES-1, matrix metalloproteinase (MMP)-2 and MMP-9, lipid, and oxidized low-density lipoprotein content. Collagen content was determined by immunohistochemistry and Western blot. Immunohistochemistry was also used to identify CD68+ macrophages, CD3+ T lymphocytes, smooth muscle cells, and HLA-DR+ inflammatory cells.

They found that diabetic plaques had more macrophages, T lymphocytes, and HLA-DR+ cells than did nondiabetic plaques. They were more immunoreactive for RAGE, activated NF-B, COX-2/ mPGES-1, and MMPs.

They concluded that in humans, "RAGE overexpression is associated with enhanced inflammatory reaction and COX-2/mPGES-1 expression in diabetic plaque macrophages, and this effect may contribute to plaque destabilization by inducing culprit metalloproteinase expression."

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