Altered expression of inflammation-related genes in human carotid atherosclerotic plaques.

Umberto Marcello Bracale, Maria Donata Di Taranto, Francesco Salvatore, Alberto Morgante, Massimo Porcellini, Umberto Marcello Bracale, Giuliana Fortunato, Massimo Porcellini, Giancarlo Bracale, Francesco Paolo D'Armiento

Risultato della ricerca: Articlepeer review

22 Citazioni (Scopus)


Inflammation is a pivotal process in atherosclerosis development and progression, but the underlying molecular mechanisms remain largely obscure. We have conducted an extensive expression study of atherosclerotic plaques to identify the inflammatory pathways involved in atherosclerosis.METHODS:We studied 11 human carotid plaques, their respective adjacent regions and 7 control arteries from different subjects. Expression of 92 genes was studied by TaqMan low-density array human inflammation panel. Human aortic endothelial and smooth muscle cells were used for in vitro experiments.RESULTS:The mRNA levels of 44/92 genes (48%) differed significantly between the tissues examined (13 up-regulated and 31 down-regulated). Dysregulated genes encode molecules belonging to different functional classes although most of them encode enzymes involved in the eicosanoid synthesis pathway. The expression of PTGIS and PTGIR genes was decreased in human aortic endothelial and smooth muscle cells stimulated with oxLDL and TNF-α.CONCLUSIONS:This study not only reveals several dysregulated genes in human lesions but also focuses the role played by the genes involved in the eicosanoid synthesis pathway during atherosclerotic development. The decrease of PTGIS and PTGIR expression after oxLDL treatment mirrors the decreased mRNA levels in atherosclerotic lesions versus control arteries, which suggests that oxidation is important for PTGIS and PTGIR regulation in human vessel cells during atherosclerosis development.
Lingua originaleEnglish
pagine (da-a)93-101
Numero di pagine9
Stato di pubblicazionePublished - 2012

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

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