Aims: Atherosclerosis is an inflammator y disease which molecular mechanisms are not been completely investigated. Our aim is to perform a wide expression study of inflammation related genes in human atherosclerotic plaques. Methods: The Human Inflammation Array (Applied Biosystems) was used to perform the mRNA quantification of 92 inflammation-related genes in 12 atherosclerotic plaques, their respective adjacent regions (with a lower grade lesion) and 7 healthy ar teries. The principle of the array is the real-time PCR amplification with a TaqMan probe specific for each gene. Data analysis was performed with SDS 2.3 software with the comparative Ct method using the gene beta-2-microglobulin as housekeeping and one of analysed samples as calibrator. Results: The mRNA levels of 42 genes result to be differently expressed:13 genes were up-regulated in atherosclerotic plaques respect to control ar teries whereas 29 were down-regulated. Their expression levels show an increasing or a decreasing trend from healthy ar teries to plaque adjacent regions and to advanced plaques. These genes belong to many different functional classes. In particular, we observed the dys-regulation of genes encoding for enzymes involved in the arachidonic acid metabolism that lead to generation of prostaglandins and leukotrienes. Conclusions: This is the first study in which the expression of a wide panel of inflammation-related genes was investigated. Results clarify the mechanisms of inflammation involvement during atherosclerotic process and highlight newpossible target for anti-inflammator y therapy in cardiovascular disease.

Di Taranto, M.D., Morgante, A., Bracale, U.M., Del Guercio, l., Carbone, F., D'Armiento, F.P., et al. (2010). Expression of inflammation-related genes in human atherosclerotic plaques. In Abstracts of the 78th EAS Congress (pp.101-101).

Expression of inflammation-related genes in human atherosclerotic plaques

BRACALE, Umberto Marcello;
2010-01-01

Abstract

Aims: Atherosclerosis is an inflammator y disease which molecular mechanisms are not been completely investigated. Our aim is to perform a wide expression study of inflammation related genes in human atherosclerotic plaques. Methods: The Human Inflammation Array (Applied Biosystems) was used to perform the mRNA quantification of 92 inflammation-related genes in 12 atherosclerotic plaques, their respective adjacent regions (with a lower grade lesion) and 7 healthy ar teries. The principle of the array is the real-time PCR amplification with a TaqMan probe specific for each gene. Data analysis was performed with SDS 2.3 software with the comparative Ct method using the gene beta-2-microglobulin as housekeeping and one of analysed samples as calibrator. Results: The mRNA levels of 42 genes result to be differently expressed:13 genes were up-regulated in atherosclerotic plaques respect to control ar teries whereas 29 were down-regulated. Their expression levels show an increasing or a decreasing trend from healthy ar teries to plaque adjacent regions and to advanced plaques. These genes belong to many different functional classes. In particular, we observed the dys-regulation of genes encoding for enzymes involved in the arachidonic acid metabolism that lead to generation of prostaglandins and leukotrienes. Conclusions: This is the first study in which the expression of a wide panel of inflammation-related genes was investigated. Results clarify the mechanisms of inflammation involvement during atherosclerotic process and highlight newpossible target for anti-inflammator y therapy in cardiovascular disease.
Settore MED/22 - Chirurgia Vascolare
giu-2010
78th EAS Congress
Hamburg, Germany
20-23 june 2010
78
2010
1
Di Taranto, M.D., Morgante, A., Bracale, U.M., Del Guercio, l., Carbone, F., D'Armiento, F.P., et al. (2010). Expression of inflammation-related genes in human atherosclerotic plaques. In Abstracts of the 78th EAS Congress (pp.101-101).
Proceedings (atti dei congressi)
Di Taranto, MD; Morgante, A; Bracale, UM; Del Guercio, l; Carbone, F; D'Armiento, FP; Porcellini, M; Bracale, G; Salvatore, F; Fortunato, G
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10447/53832
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