The aim of this work was to evaluate whether smoke cessation may result in changes in monocyte biglycan (BGN)-mRNA expression in young smokers without additional CAD risk factors, with or without increased carotid intima-media thickness (cIMT). Monocyte expression of BGN, a multivalent proteoglycan providing structure and signals, is enhanced in subjects with CAD risk factors. Seventy-ve cigarette smokers (mean age 24.9±3.6 years) and 60 matched controls were enrolled. Smokers were divided into 3 groups stratied for cIMT values (G1: 0.99 mm; G2: 1 mm <1.3, G3 1.3 mm, respectively). Plasma concentrations of interleukin-6 (IL-6), C-reactive protein (hs-CRP), brinogen and lipids, blood pressure (BP) and BGN-mRNA in circulating monocytes were measured at baseline (T0) and after 9-months smoke cessation (T1). To evaluate the inuence of smoking on study parameters a score of smoke exposure was estimated (SEIx). Arterial stiffness (AS) values (AIx and PWV) were also measured. At baseline,fibrinogen, CRP, BGN-mRNA values were higher in smokers than controls, while HDL-C was lower; this difference was enhanced in G2 and particularly in G3. Diastolic BP (DBP) was increased in G2 and G3 and IL-6 in G3. At T1, in each of three groups, brinogen, CRP and IL-6 were reduced with respect to baseline, and HDL-C was increased. DBP was reduced in G2 and G3; BGN-mRNA were decreased in G1 and G2, while it did remain unchanged in G3. AIx and PWV were reduced in G1 and G2 with respect to baseline, whereas in G3 they remained unchanged. The regression analysis suggested that at T0 the main predictors for BGN-mRNA were inammation and SEIx, and that at T1 BGN-mRNA was associated with PWV, HDL-C and DBP. These ndings suggest that smoke cessation may reduce the expression of monocyte BGN-mRNA and improve pro-atherogenic prole, particularly in subjects presenting with an earlier vascular involvement.

EARLIER VASCULAR DAMAGE IS ASSOCIATED WITH A MORE BENEFICIAL IMPROVEMENT OF PRO-ATHEROGENIC PROFILE AFTER SMOKE CESSATION

ARAGONA, CATERINA ORIANA;MANDRAFFINO, GIUSEPPE;MAMONE, FEDERICA;CAIRO, VALENTINA;RUSSO, MASSIMILIANO;SARDO, Maria Adriana;SAITTA, Antonino
2013-01-01

Abstract

The aim of this work was to evaluate whether smoke cessation may result in changes in monocyte biglycan (BGN)-mRNA expression in young smokers without additional CAD risk factors, with or without increased carotid intima-media thickness (cIMT). Monocyte expression of BGN, a multivalent proteoglycan providing structure and signals, is enhanced in subjects with CAD risk factors. Seventy-ve cigarette smokers (mean age 24.9±3.6 years) and 60 matched controls were enrolled. Smokers were divided into 3 groups stratied for cIMT values (G1: 0.99 mm; G2: 1 mm <1.3, G3 1.3 mm, respectively). Plasma concentrations of interleukin-6 (IL-6), C-reactive protein (hs-CRP), brinogen and lipids, blood pressure (BP) and BGN-mRNA in circulating monocytes were measured at baseline (T0) and after 9-months smoke cessation (T1). To evaluate the inuence of smoking on study parameters a score of smoke exposure was estimated (SEIx). Arterial stiffness (AS) values (AIx and PWV) were also measured. At baseline,fibrinogen, CRP, BGN-mRNA values were higher in smokers than controls, while HDL-C was lower; this difference was enhanced in G2 and particularly in G3. Diastolic BP (DBP) was increased in G2 and G3 and IL-6 in G3. At T1, in each of three groups, brinogen, CRP and IL-6 were reduced with respect to baseline, and HDL-C was increased. DBP was reduced in G2 and G3; BGN-mRNA were decreased in G1 and G2, while it did remain unchanged in G3. AIx and PWV were reduced in G1 and G2 with respect to baseline, whereas in G3 they remained unchanged. The regression analysis suggested that at T0 the main predictors for BGN-mRNA were inammation and SEIx, and that at T1 BGN-mRNA was associated with PWV, HDL-C and DBP. These ndings suggest that smoke cessation may reduce the expression of monocyte BGN-mRNA and improve pro-atherogenic prole, particularly in subjects presenting with an earlier vascular involvement.
2013
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/2636569
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