2006

DOI: 10.2337/diabetes.55.03.06.db05-0832

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The Ubiquitin-Proteasome System and Inflammatory Activity in Diabetic Atherosclerotic Plaques

Raffaele Marfella

¹

,

Michele D’Amico²,

Katherine Esposito

³

et al.

Abstract: The role of ubiquitin-proteasome system in the accelerated atherosclerotic progression of diabetic patients is unclear. We evaluated ubiquitin-proteasome activity in carotid plaques of asymptomatic diabetic and nondiabetic patients, as well as the effect of rosiglitazone, a peroxisome proliferator-activated receptor (

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Cited by 104 publications

(77 citation statements)

References 42 publications

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“…It was reported that PSMA6 had a functional relation with LTA, 7 whose sequence variations were associated with the severity of atherosclerosis. 8 In addition, PSMA6 was reported to be involved in the diabetic atherosclerosis, 16 and the association of À8GG genotype with the thickness of intima-media in carotid artery was recently Table 2 Association between CAD and PSMA6 -8C4G (rs1048990) Figure 1 Meta-analysis of data from replication studies for the association between PSMA6 À8C4G and CAD. Odds ratio and 95% confidence interval (95% CI) are schematically indicated for each replication study.…”

Section: Resultsmentioning

confidence: 99%

Replication studies for the association of PSMA6 polymorphism with coronary artery disease in East Asian populations

¹

,

²

,

³

et al. 2009

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Coronary artery disease (CAD) has become a major health problem in many countries because of its increasing prevalence and high mortality. Recently, an association of a functional sequence variation, À8C4G, in the human proteasome subunit a type 6 gene (PSMA6) with the susceptibility to CAD was reported. To validate the association, we investigated a total of 1330 cases and 2554 controls from Japanese and Korean populations for PSMA6 genotypes, and no evidence of the association was obtained in both Japanese (odds ratio (OR)¼1.03, 95% confidence interval (CI); 0.90-1.19, P¼0.66, allele count model) and Korean populations (OR¼1.00, 95% CI; 0.86-1.17, P¼0.95, allele count model). However, when a meta-analysis of data from this study and previously reported six replication studies was done, OR was 1.08 for the G allele (95% CI; 1.02-1.14, P¼0.0057), suggesting that the contribution of PSMA6 to CAD was not large enough to be readily replicated. Further studies are required to establish the contribution of this variant in the susceptibility to CAD.

“…It was reported that PSMA6 had a functional relation with LTA, 7 whose sequence variations were associated with the severity of atherosclerosis. 8 In addition, PSMA6 was reported to be involved in the diabetic atherosclerosis, 16 and the association of À8GG genotype with the thickness of intima-media in carotid artery was recently Table 2 Association between CAD and PSMA6 -8C4G (rs1048990) Figure 1 Meta-analysis of data from replication studies for the association between PSMA6 À8C4G and CAD. Odds ratio and 95% confidence interval (95% CI) are schematically indicated for each replication study.…”

Section: Resultsmentioning

confidence: 99%

Replication studies for the association of PSMA6 polymorphism with coronary artery disease in East Asian populations

¹

,

²

,

³

et al. 2009

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Coronary artery disease (CAD) has become a major health problem in many countries because of its increasing prevalence and high mortality. Recently, an association of a functional sequence variation, À8C4G, in the human proteasome subunit a type 6 gene (PSMA6) with the susceptibility to CAD was reported. To validate the association, we investigated a total of 1330 cases and 2554 controls from Japanese and Korean populations for PSMA6 genotypes, and no evidence of the association was obtained in both Japanese (odds ratio (OR)¼1.03, 95% confidence interval (CI); 0.90-1.19, P¼0.66, allele count model) and Korean populations (OR¼1.00, 95% CI; 0.86-1.17, P¼0.95, allele count model). However, when a meta-analysis of data from this study and previously reported six replication studies was done, OR was 1.08 for the G allele (95% CI; 1.02-1.14, P¼0.0057), suggesting that the contribution of PSMA6 to CAD was not large enough to be readily replicated. Further studies are required to establish the contribution of this variant in the susceptibility to CAD.

“…We reported previously that oxidative stress-dependent UPS overactivity contributes to the clinical instability of atherosclerotic plaques in hypertensive, 15 diabetic, 16 and symptomatic patients 17 by promoting plaque rupture induced by NF-B-dependent inflammation. Now, in the present report, we provide evidence for the critical involvement of UPS in the process of plaque stabilization realized by HRT in postmenopausal women.…”

Section: Discussionmentioning

confidence: 99%

Proteasome Activity as a Target of Hormone Replacement Therapy–Dependent Plaque Stabilization in Postmenopausal Women

et al. 2008

Self Cite

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Abstract-The molecular mechanisms of the atheroprotective effect evoked by hormone replacement therapy in postmenopausal women is not well known. Recently, we have demonstrated enhanced activity of the ubiquitinproteasome system in human atherosclerotic plaques and evidenced that it is associated with inflammatory-induced plaque rupture. Therefore, we hypothesized that hormone replacement therapy may exert the cardioprotective effects modulating the ubiquitin-proteasome activity. To investigate this possibility, this study examined the differences in inflammatory infiltration, as well as ubiquitin-proteasome activity, between asymptomatic carotid plaques of postmenopausal women with and without concomitant hormone replacement therapy. Plaques were obtained from 20 postmenopausal women treated with hormone replacement therapy (current users) and 32 nontreated women (never-users) enlisted to undergo carotid endarterectomy for extracranial high-grade (Ͼ70%) internal carotid artery stenosis. Plaques were analyzed for macrophages, T lymphocytes, human leukocyte antigen-DRϩ cells, ubiquitinproteasome system, nuclear factor B, inhibitor of nuclear factor B␤, tumor necrosis factor-␣, nitrotyrosine, matrix metalloproteinase-9, and collagen content (immunohistochemistry and ELISA). Compared with plaques from current users, plaques from never-users had more macrophages, T lymphocytes, and human leukocyte antigen-DRϩ cells (PϽ0.001); more ubiquitin-proteasome activity, tumor necrosis factor-␣, and nuclear factor B (PϽ0.001); and more nitrotyrosine and matrix metalloproteinase-9 (PϽ0.001), along with a lesser collagen content and inhibitor of nuclear factor B␤ levels (PϽ0.001). This study supports the hypothesis that hormone replacement therapy inhibits plaque ubiquitin-proteasome activity by decreasing oxidative stress generation in postmenopausal women. This effect, in turn, might contribute to plaque stabilization by inhibiting the activation of nuclear factor B-dependent inflammation, responsible for plaque rupture. Key Words: hormone replacement therapy Ⅲ atherosclerotic plaque Ⅲ inflammation Ⅲ ubiquitin-proteasome activity C ardiovascular disease is the leading cause of death in postmenopausal women. 1,2 There is a strong link between menopause and an increased incidence of cardiovascular disease, and observational studies suggest that postmenopausal hormone therapy, including various estrogen preparations with or without a progestin (most commonly a synthetic progestin), reduces cardiovascular disease risk by about half. 2,3 Hormone replacement therapy (HRT) use was also associated with a lesser extent of angiographically assessed coronary atherosclerosis. 4,5 An atheroprotective effect of estrogens is plausible and is especially attributed to a direct effect on the arterial wall, an antioxidant action, and a favorable effect on inflammation. 6 In prospective studies, administration of ovarian hormones to postmenopausal women has been shown to decrease oxidative stress markers, such as superoxide anion and peroxynitri...

“…PPAR␥ can be activated by synthetic agonists belonging the family of thiazolidinediones, for instance rosiglitazone (RZ) (Mohanty et al, 2004). Recent studies performed in diabetic patients have shown that RZ reduces the inflammatory markers (Marfella et al, 2006), and it reduces blood pressure in hypertensive transgenic mice characterized by human renin and angiotensin overexpression (Ryan et al, 2004). These data suggest a protective role for PPAR␥ agonists in cardiovascular diseases because of their anti-inflammatory properties.…”

mentioning

confidence: 97%

Rosiglitazone, a Peroxisome Proliferator-Activated Receptor-γ Agonist, Prevents Microparticle-Induced Vascular Hyporeactivity through the Regulation of Proinflammatory Proteins

Al-Massarani²,

et al. 2007

J Pharmacol Exp Ther

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Microparticles are plasma membrane vesicles with procoagulant and proinflammatory properties. We recently demonstrated that microparticles induce vascular hyporeactivity and evoke up-regulation of proinflammatory protein expression. This study dissected the effect of either in vitro treatment or short-term oral administration of the peroxisome proliferator-activated receptor-␥ (PPAR␥) agonist, rosiglitazone, on microparticle-induced vascular hyporeactivity of mouse vessels. Microparticles were produced from T cells by actinomycin D treatment. The effects of rosiglitazone on mouse aortic rings incubated with microparticles were investigated. Aortae treated in vitro with rosiglitazone or aortae taken from mice treated by oral administration of the same agonist completely prevented microparticle-induced vascular hyporeactivity in response to U46619 [9,11-dideoxy-11␣,9␣-epoxymethanoprostaglandin F 2␣ ). These effects of rosiglitazone occurred independently of the presence of endothelium without modifications in blood parameters. The mechanisms involved abrogation of nitric oxide (NO) and prostacyclin overproduction linked to up-regulation of inducible NO-synthase and cyclooxygenase 2 elicited by microparticles. In addition, rosiglitazone treatment reduced the ability of microparticles to evoke increases in interleukin (IL)-6, IL-8, and nuclear factor (NF)-B transcription, and NF-B expression and activation. These results suggest that rosiglitazone, via PPAR␥ activation, counteracts vascular dysfunction associated with increased release of proinflammatory proteins elicited by microparticles. They underscore therapeutic perspective for rosiglitazone in vascular diseases involving enhanced participation of microparticles.

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