Modulatory effect of sera from scleroderma patients on lymphocyte‐induced angiogenesis

Majewski, Sławomir; Skopińska-Różewska, Ewa; Jabłońska, Stefania; Polakowski, Igor; Pawinska, M.; Marczak, Maria; Szmurło, A.

doi:10.1002/art.1780281009

Cited by 24 publications

(12 citation statements)

References 25 publications

(5 reference statements)

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“…Several studies have demonstrated angiogenesis-related abnormalities, including decreased monocyte-mediated angiogenesis (35) and the presence of proangiogenic and antiangiogenic factors in SSc serum (36), including increased levels of circulating endostatin (37,38). At the same time, SSc serum was reported to enhance the angiogenic capability of circulating mononuclear cells (39). Finally, a recent gene expression study comparing transcriptomes of microvascular endothelial cells from normal control subjects and patients with SSc demonstrated overexpression of proangiogenic transcripts and both up-regulation of suppressor genes and downregulation of activator genes regulating cell migration in SSc endothelial cells (40).…”

Section: Discussionmentioning

confidence: 99%

Antiangiogenic plasma activity in patients with systemic sclerosis

Mulligan-Kehoe¹,

Drinane²,

Mollmark³

et al. 2007

Arthritis & Rheumatism

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Objective. Systemic sclerosis (SSc; scleroderma) is a systemic connective tissue disease with an extensive vascular component that includes aberrant microvasculature and impaired wound healing. The aim of this study was to investigate the presence of antiangiogenic factors in patients with SSc.Methods. Plasma samples were obtained from 30 patients with SSc and from 10 control patients without SSc. The samples were analyzed for the ability of plasma to affect endothelial cell migration and vascular structure formation and for the presence of antiangiogenic activity.Results. Exposure of normal human microvascular dermal endothelial cells to plasma from patients with SSc resulted in decreased cell migration (mean ؎ SEM 52 ؎ 5%) and tube formation (34 ؎ 6%) compared with that in plasma from control patients (P < 0.001 for both). SSc plasma contained 2.9-fold more plasminogen kringle 1-3 fragments (angiostatin) than that in control plasma. The addition of angiostatin to control plasma resulted in inhibition of endothelial cell migration and proliferation similar to that observed in SSc plasma. In vitro studies demonstrated that granzyme B and other proteases contained in T cell granule content cleave plasminogen and plasmin into angiostatin fragments.Conclusion. Plasminogen conformation in patients with SSc enables granzyme B and granule content protease to limit the proangiogenic effects of plasmin and increase the levels of antiangiogenic angiostatin. This increase in angiostatin production may account for some of the vascular defects observed in patients with SSc.

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Section: Discussionmentioning

confidence: 99%

Antiangiogenic plasma activity in patients with systemic sclerosis

Mulligan-Kehoe¹,

Drinane²,

Mollmark³

et al. 2007

Arthritis & Rheumatism

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“…Kaminski et al [19] isolated and purified lymphocytes from patients with SSc and showed that they exhibited less angiogenic activity than peripheral blood lymphocytes from healthy volunteers. These authors also showed that serum from SSc patients did not affect normal lymphocytemediated angiogenesis, but paradoxically, serum from patients with acrosclerosis markedly enhanced the angiogenic ability of healthy lymphocytes [20]. In addition, they demonstrated that semipurified SSc monocytes had enhanced angiogenic activity compared with healthy ones.…”

Section: Systemic Sclerosis Angiogenesis: Early Findingsmentioning

confidence: 93%

Angiogenesis and Vasculopathy in Systemic Sclerosis: Evolving Concepts

Rabquer

Koch

2011

Curr Rheumatol Rep

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Systemic sclerosis (scleroderma [SSc]) is a multifactorial disease characterized by inflammation, extensive and progressive fibrosis, and multiple vasculopathies. The vascular manifestations can be seen early in the pathogenesis of the disease and include malformed capillaries, Raynaud's phenomenon, and digital ulcers. As the disease progresses, the vasculopathy proceeds to significant clinical manifestations, including renal crisis and pulmonary arterial hypertension. Moreover, later stages of the disease are marked by increasingly avascular areas. Despite the obliteration of microvascular structures, compensatory vasculogenesis and angiogenesis do not occur normally. This is in spite of a general increase in many potent angiogenic factors. Recent studies are beginning to examine this paradox and subsequent paucity of an angiogenic response in SSc. In this review, we discuss these findings and examine the role that chemokine and growth factor receptors, proteases, adhesion molecules, and transcription factors play in the dysregulation of angiogenesis in SSc.

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“…All patients were evaluated for internal organ involvement according to criteria given previously [9]. Antinuclear antibodies were measured by indirect immunofluorescence of HEp-2 cels [22,23].…”

Section: Methodsmentioning

confidence: 99%

“…It has been shown, for example, that serum factors from patients with acroscleroderma but not with diffuse scleroderma markedly enhance production of angiogenic lymphokines by normal human peripheral blood mononuclear cells [9].…”

Section: Introductionmentioning

confidence: 99%

Cytotoxic effects of sera from patients with systemic scleroderma: Comparison of three different in vitro methods

Majewski¹,

Błaszczyk²,

Jabłońska³

et al. 1990

Rheumatol Int

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Sera from 93 patients with systemic scleroderma including incipient or prodromal acroscleroderma and from 43 healthy individuals were studied for cytotoxic effects on endothelial cells by means of three different in vitro methods. Inhibition of 3H-thymidine incorporation by endothelium was caused by about 33% of sera, almost exclusively from patients with diffuse scleroderma and the transitional form: acroscleroderma--diffuse scleroderma. An antibody-dependent cellular cytotoxicity assay revealed cytotoxicity of about 37% of sera from patients with diffuse scleroderma and the transitional form but also of a proportion of sera from patients with CREST syndrome with pronounced vascular changes. Serum cytotoxic activity, revealed by both methods, was related with more frequent involvement of muscle and kidney in the patients. A direct 51Cr release assay showed the cytotoxicity only in 4 of 68 cases in diffuse scleroderma with pronounced internal organ involvement. Thus, depending on the method used, various types of cytotoxicity could be detected in sera from patients with systemic scleroderma.

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Modulatory effect of sera from scleroderma patients on lymphocyte‐induced angiogenesis

Cited by 24 publications

References 25 publications

Antiangiogenic plasma activity in patients with systemic sclerosis

Antiangiogenic plasma activity in patients with systemic sclerosis

Angiogenesis and Vasculopathy in Systemic Sclerosis: Evolving Concepts

Cytotoxic effects of sera from patients with systemic scleroderma: Comparison of three different in vitro methods

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