Cytokines from activated T cells induce normal endothelial cells to acquire the phenotypic and functional features of AIDS-Kaposi's sarcoma spindle cells.

Fiorelli, Valeria; Gendelman, Rita; Samaniego, Felipe; Markham, Phillip D.; Ensoli, Barbara

doi:10.1172/jci117849

Cited by 148 publications

(103 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the concentration of oncostatin M in focal lesions that contain activated T cells or macrophages could be much higher than circulating levels. For example, conditioned medium from HTLV-II infected T cells contains 20 to 45 nM oncostatin M (15). Thus the local concentrations of macrophage-like cells in aneurysmal tissue that stained heavily for oncostatin M, or the localized production of oncostatin M in the lesions of AIDS-associated Kaposi's sarcoma (7,39) may allow the low affinity oncostatin M receptor to participate in endothelial cell activation.…”

Section: Discussionmentioning

confidence: 99%

“…Second, endothelial cells respond to oncostatin M with activation of MAP kinase activity (11), IL-6 secretion (9), and delayed, but prolonged, P-selectin synthesis (12). Third, oncostatin M is the major autocrine growth factor for Kaposi's sarcoma cells (13), and these spindle-shaped cells are thought to be of endothelial cell origin (14,15).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Modur¹,

Feldhaus²,

Weyrich³

et al. 1997

J. Clin. Invest.

181

139

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Modur¹,

Feldhaus²,

Weyrich³

et al. 1997

J. Clin. Invest.

181

139

View full text Add to dashboard Cite

show abstract

“…However, one of the most relevant targets for Tat is the vascular system, where it activates a pro-inflammatory and angiogenic program. Tat can up-regulate the expression of EC adhesion molecules [69,70] and induces EC to proliferate, release proteolytic enzymes [71][72][73][74][75][76][77][78][79]. These effects are potentiated by cell priming with inflammatory cytokines [71,72,80].…”

Section: Indirect Effect Of Hiv-1 On Ec Behavior: the Role Of Tatmentioning

confidence: 99%

Interactions between endothelial cells and HIV-1

Bussolino

Mitola

Serini

et al. 2001

The International Journal of Biochemistry &Amp; Cell Biology

View full text Add to dashboard Cite

Endothelial cells (EC) participate in inflammatory and immune reactions by producing and responding to soluble mediators. Human immunodeficiency virus (HIV)-1 profoundly alters the features of EC. In some anatomical districts, they are infected by the virus and may represent a relevant reservoir. During lymphomononuclear cell diapedesis, EC activate virus replication in crossing cells. Direct or indirect damage of EC is particularly relevant in central nervous system, where blood-brain barrier perturbation is pivotal in neuronal degeneration. The observed alterations of EC adhesive properties contribute in altered leukocyte traffic from blood to lymphoid organs and tissues and play a role in the onset of immune surveillance alteration. These alterations of EC functions are relevant for the general vasculopathy, which marks the acquired immunodeficiency syndrome, and in particular are instrumental in the pathogenesis of Kaposi's sarcoma. Here we discuss the biological and molecular activation of EC in HIV-1 infection that represents the basis to understand the pathogenesis of HIV-1 associated vascular diseases.

show abstract

“…12 The physiopathological significance of the proliferative effect of OSM on vascular cells is strengthened by the fact that OSM is 1 of the most potent stimulators of Kaposi sarcoma cell growth, 41,42 since some authors have demonstrated that Kaposi sarcoma spindle cells can be derived from endothelial cells 43 activated by proinflammatory cytokines. 44 The physiological significance of the angiogenic property of LIF can be considered in embryonic genesis, since Gendron et al 45 have demonstrated that LIF, in combination with bFGF, contributes to the induction and support of embryonic vasculogenesis in vitro and in vivo after blastocyte injection. However, compared with OSM, LIF does not seem to be involved in vessel wall injury leading to atherosclerotic development but could have a protective effect in atherosclerosis as shown by Moran et al 46 in hyperlipidemic rabbits.…”

Section: Vasse Et Almentioning

confidence: 99%

Oncostatin M Induces Angiogenesis In Vitro and In Vivo

Vasse

Pourtau

Trochon

et al. 1999

ATVB

121

101

View full text Add to dashboard Cite

Abstract-Neovascularization of the atherosclerotic plaque is responsible for its weakening and consequently for the complications of vascular disease. Macrophages are a source of growth factors that can modulate angiogenesis. In this study, we analyzed the effect of oncostatin M (OSM) on angiogenesis, as it could be involved in the development of atherosclerosis. The effect of OSM was compared with those of leukemia inhibitory factor (LIF) and interleukin-6 (IL-6). On human dermal microvasculature endothelial cells (HMEC-1s), OSM (22.5 to 112.5 pmol/L) induced a dose-dependent increase in cell proliferation greater than that induced by the classic angiogenic factors vascular endothelial growth factor (VEGF; 543 pmol/L) and basic fibroblast growth factor (bFGF; 1.1 nmol/L). LIF (19 to 475 pmol/L) induced only a 30% increase in cell proliferation, and IL-6 had no effect. Furthermore, in a modified Boyden-chamber model, OSM, LIF, and IL-6 were chemoattractant for HMEC-1s. In a tridimensional gel of fibrin, OSM increased tube formation and tube length, which were already noticeable by day 3. LIF and IL-6 induced a weaker effect that was only obvious by day 10. The angiogenic effect of OSM was also demonstrated in vivo in a rabbit corneal model: OSM was more potent than LIF, the length of the neovessels being longer with OSM than with LIF, whereas IL-6 was without effect. We tested factors that could be involved in the proliferative effect of OSM on HMEC-1s. OSM induced only a slight increase in the urokinase receptor and a 60% increase in VEGF secretion, whereas it does not modify IL-8 secretion or bFGF levels. The effect of OSM seems to depend on endothelial cell origin and cell species: OSM (up to 112.5 pmol/L) did not induce human umbilical vein endothelial cell proliferation and even had a small inhibitory effect (17%) on calf pulmonary artery endothelial cells. In conclusion, OSM induces an angiogenic effect on capillary endothelial cells, which could be, at least in part, implicated in pathological processes such as atherosclerosis or tumor growth. Key Words: angiogenesis Ⅲ atherosclerosis Ⅲ oncostatin M Ⅲ leukemia inhibitory factor Ⅲ vascular endothelial growth factor I t is now established that the functional role of the macrophage extends far beyond its originally recognized role as a scavenger cell. Monocytes in particular are recognized as angiogenesis effector cells that produce a number of growth stimulators and inhibitors, proteolytic enzymes, and cytokines that can influence 1 or more steps in the angiogenesis cascade. It has been shown that activated monocytes or their culture supernatants induce new capillary growth in vitro and angiogenesis in vivo. 1,2 However, recent evidence also suggests that capillary regression may be mediated by monocytes by producing antiangiogenic factors in vitro and in vivo. [3][4][5] Thus, macrophages could be involved in both stimulation and suppression of angiogenesis.Because macrophages reside at the sites of atherosclerotic plaques in the vessel wall and because the...

show abstract

Cytokines from activated T cells induce normal endothelial cells to acquire the phenotypic and functional features of AIDS-Kaposi's sarcoma spindle cells.

Cited by 148 publications

References 62 publications

Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Interactions between endothelial cells and HIV-1

Oncostatin M Induces Angiogenesis In Vitro and In Vivo

Contact Info

Product

Resources

About