Translational Mini-Review Series on Immunology of Vascular Disease: Mechanisms of vascular inflammation and remodelling in systemic vasculitis

Maugeri, Norma; Rovere‐Querini, Patrizia; Baldini, Mattia; Sabbadini, M G; Manfredi, Angelo A.

doi:10.1111/j.1365-2249.2009.03921.x

Cited by 49 publications

(48 citation statements)

References 101 publications

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“…Patients with past optic nerve ischemia, defined as an event that occurred Ͼ6 months before blood samples were obtained (n ϭ 6) (patients 1,6,8,12,14, and 25 in Table 1), had a mean Ϯ SEM blood PTX3 level of 2.76 Ϯ 0.35 ng/ml, which was not significantly different from the mean Ϯ SEM blood PTX3 level in GCA patients who had symptoms of long-standing duration (Ͼ6 months) but no optic nerve ischemia (mean Ϯ SEM 4.57 Ϯ 1.06 ng/ml; n ϭ24) and in control groups. In the group of patients with a history of optic nerve ischemia (very recent, recent, or past) (Table 1), a significant correlation was found between circulating PTX3 levels and ESR and CRP but not between PTX3 levels and daily prednisone dosage ( Figure 3A).…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, it is involved in the modulation of the innate response associated with ongoing cell death (9,10) and interacts with the extracellular matrix, contributing to the assembly of the cumulus oophorus (11). PTX3 synthesis is a hallmark of vascular injury (12). It occurs in atherosclerotic lesions (13)(14)(15)(16), as a response to acute mechanical damage of the vessel wall, such as that associated with coronary stenting (17), and during acute myocardial infarction (18,19).…”

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confidence: 99%

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Selective up‐regulation of the soluble pattern‐recognition receptor pentraxin 3 and of vascular endothelial growth factor in giant cell arteritis: Relevance for recent optic nerve ischemia

Baldini

Maugeri

Ramirez

et al. 2012

Arthritis & Rheumatism

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Objective. To assess local expression and plasma levels of pentraxin 3 (PTX3) in patients with giant cell arteritis (GCA).Methods. Plasma and serum samples were obtained from 75 patients with GCA (20 of whom had experienced optic nerve ischemia in the previous 3 weeks and 24 of whom had experienced symptom onset in the previous 6 months and had no history of optic nerve ischemia) and 63 controls (35 age-matched healthy subjects, 15 patients with rheumatoid arthritis, and 13 patients with chronic stable angina). In 9 patients in whom GCA was recently diagnosed, circulating levels of interleukin-1␤ (IL-1␤), IL-2, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12p70, CCL2/monocyte chemotactic protein 1, CCL3/macrophage inflammatory protein 1␣ (MIP-1␣), CCL4/MIP-1␤, CCL11/eotaxin, CXCL9/ monokine induced by interferon-␥, CXCL10/interferon-␥-inducible 10-kd protein, tumor necrosis factor ␣ (TNF␣), interferon-␥, vascular endothelial growth factor (VEGF), granulocyte-macrophage colonystimulating factor, and FasL were measured via a multiplexed cytometric assay. PTX3 and VEGF concentrations were assessed by enzyme-linked immunosorbent assay. PTX3 and CD68 expression were determined by immunohistochemistry and immunofluorescence on temporal artery samples.Results. GCA patients with very recent optic nerve ischemia had significantly higher PTX3 and VEGF levels compared to other GCA patients and controls. GCA patients with a disease duration of <6 months had significantly higher PTX3 levels compared to other GCA patients and controls. Immunohistochemistry revealed selective PTX3 expression in the wall of inflamed arteries.Conclusion. Our findings indicate that local expression of PTX3 is a feature of vascular inflammation in GCA; elevated circulating levels of PTX3 identify patients with very recent optic nerve ischemia or a recent diagnosis. Optic nerve ischemia is also associated with increased circulating VEGF levels.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Selective up‐regulation of the soluble pattern‐recognition receptor pentraxin 3 and of vascular endothelial growth factor in giant cell arteritis: Relevance for recent optic nerve ischemia

Baldini

Maugeri

Ramirez

et al. 2012

Arthritis & Rheumatism

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show abstract

“…Remarkably, relatively few studies have been published on the occurrence of accelerated atherosclerosis in patients with vasculitis, a typical chronic vascular inflammatory disease. The mechanism of vascular damage in vasculitis is the subject of a complementary review in this series [19]. In the present paper we discuss data on the prevalence and pathophysiology of atherosclerosis in vasculitis.…”

Section: Introductionmentioning

confidence: 95%

Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitis

Tervaert

2009

Clinical and Experimental Immunology

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SummaryPremature atherosclerosis has been observed during the course of different systemic inflammatory diseases such as rheumatoid arthritis and sytemic lupus erythematosus. Remarkably, relatively few studies have been published on the occurrence of accelerated atherosclerosis in patients with vasculitis. In giant cell arteritis (GCA), mortality because of ischaemic heart disease is not increased. In addition, intima media thickness (IMT) is lower in patients with GCA than in age-matched controls. In contrast, IMT is increased significantly in Takayasu arteritis, another form of large vessel vasculitis occurring in younger patients. In Takayasu arteritis and in Kawasaki disease, a form of medium-sized vessel vasculitis, accelerated atherosclerosis has been well documented. In small vessel vasculitis because of anti-neutrophil cytoplasmic autoantibodies-associated vasculitis, cardiovascular diseases are a major cause of mortality. IMT measurements reveal conflicting results. During active disease these patients experience acceleration of the atherosclerotic process. However, when inflammation is controlled, these patients have atherosclerotic development as in healthy subjects. Several risk factors, such as diabetes and hypertension, are present more often in patients with vasculitis compared with healthy controls. In addition, steroids may be pro-atherogenic. Most importantly, many patients have impaired renal function, persistent proteinuria and increased levels of C-reactive protein, well-known risk factors for acceleration of atherosclerosis. Enhanced oxidation processes, persistently activated T cells and reduced numbers of regulatory T cells are among the many pathophysiological factors that play a role during acceleration of atherogenesis. Finally, autoantibodies that may be relevant for acceleration of atherosclerosis are found frequently in elevated titres in patients with vasculitis. Because patients have an increased risk for cardiovascular events, vasculitis should be treated with as much care as possible. In addition, treatment should be considered with angiotensin-converting-enzyme inhibitors and/or angiotensin receptor-1 blockers, statins and acetylsalicyl acid. Finally, classical risk factors for cardiovascular disease should be monitored and treated as much as possible.

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“…NF-κB is considered as a primary regulator of inflammatory processes, and its activation leads to high expression of adhesion molecules, including ICAM-1 and MCP-1, in endothelial cells. ICAM-1 facilitates adhesion to endothelial cells and trans-endothelial migration of leukocytes (31). The activation of adhesion molecules results in the expression of MCP-1, promoting the monocyte migration to the intima (32).…”

Section: Discussionmentioning

confidence: 99%

DL-3-n-butylphthalide protects endothelial cells against advanced glycation end product-induced injury by attenuating oxidative stress and inflammation responses

Liu

Zhao

Chen

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Endothelial dysfunction, regarded as a key step in the pathophysiological course of diabetic vascular complications, is initiated and deteriorated by advanced glycation end products (AGEs). DL-3-n-butylphthalide (DL-NBP) has been proven to have protective effects on neurons and vascular endothelial cells against ischemic and anoxic damage. The aim of the present study was to investigate whether NBP is able to attenuate AGE-induced endothelial dysfunction in vitro, and also elucidate the possible underlying mechanism. An injury model of human umbilical vein endothelial cells (HUVECs) induced by AGEs (200 µg/ml) was established. The results demonstrated that pretreatment with NBP (1-100 µM) significantly increased HUVEC viability and inhibited the apoptosis induced by AGEs. In addition, AGEs stimulated the expression levels of the receptor for AGEs protein and the downstream protein nuclear factor-κB in HUVECs, which were inhibited by pretreatment with NBP. Furthermore, it significantly reduced reactive oxygen species generation and the level of the inflammatory cytokines, intercellular cell adhesion molecule-1 and monocyte chemotactic protein-1, in HUVECs mediated by AGEs. The current findings indicated that NBP attenuated AGE-induced endothelial dysfunction by ameliorating inflammation and oxidative stress responses.

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Translational Mini-Review Series on Immunology of Vascular Disease: Mechanisms of vascular inflammation and remodelling in systemic vasculitis

Cited by 49 publications

References 101 publications

Selective up‐regulation of the soluble pattern‐recognition receptor pentraxin 3 and of vascular endothelial growth factor in giant cell arteritis: Relevance for recent optic nerve ischemia

Selective up‐regulation of the soluble pattern‐recognition receptor pentraxin 3 and of vascular endothelial growth factor in giant cell arteritis: Relevance for recent optic nerve ischemia

Translational Mini-Review Series on Immunology of Vascular Disease: Accelerated atherosclerosis in vasculitis

DL-3-n-butylphthalide protects endothelial cells against advanced glycation end product-induced injury by attenuating oxidative stress and inflammation responses

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