Modulation of monocyte adherence to endothelial cells by endothelin-1 involvement of Src (p60src) and JAK1-like kinases

Chisholm, Lindsey; Dovgan, Peter S.; Agrawal, Devendra K.; McGregor, Patrick E.; Edwards, John D.

doi:10.1016/s0741-5214(96)70273-2

Cited by 13 publications

(9 citation statements)

References 32 publications

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“…Therefore, in the setting of increased pulmonary endothelial ET B receptor levels in portal hypertension, small changes in ET-1 levels are likely to have significant effects on eNOS. In addition to effects on pulmonary eNOS, we also find that circulating ET-1 modulates plasma TNF-␣ levels and intravascular macrophage accumulation in the lung in PVL animals, a finding consistent with the ability of ET-1 to influence TNF-␣ expression and monocyte adherence in vitro (5,43). The observation that our low concentration ET-1 infusion did not alter systemic or portal pressures and did not influence circulating endotoxin levels supports that effects were not due to splanchnic vasoconstriction modulating intestinal permeability.…”

Section: Discussionsupporting

confidence: 80%

“…Our finding that exogenous administration of ET-1 to PVL animals influences both circulating TNF-␣ levels and pulmonary intravascular macrophage accumulation during the development of HPS is consistent with this concept and with a growing body of evidence. ET-1 has been shown to modify monocyte adhesion by both direct effects on monocytes as well as by modulation of cell adhesion molecule and macrophage chemokine expression and NO production in endothelial cells (5,18,20,23). In addition, ET-1 can increase TNF-␣ production by macrophages (43).…”

Section: Discussionmentioning

confidence: 99%

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ET-1 and TNF-α in HPS: analysis in prehepatic portal hypertension and biliary and nonbiliary cirrhosis in rats

Luo¹,

Liu²,

Tang³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

103

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Common bile duct ligation (CBDL) triggers a molecular cascade resulting in the hepatopulmonary syndrome (HPS). Both increased hepatic endothelin-1 (ET-1) production and pulmonary vascular ET(B) receptor expression with stimulation of endothelial nitric oxide synthase and TNF-alpha mediated inducible nitric oxide synthase and heme oxygenase-1 expression in pulmonary intravascular macrophages occur. Whether biliary cirrhosis is unique in triggering ET-1 and TNF-alpha alterations and HPS is unknown. We evaluated for HPS in rat prehepatic portal hypertension [partial portal vein ligation (PVL)], biliary (CBDL) and nonbiliary [thioacetamide treatment (TAA)] cirrhosis, and assessed ET-1 infusion in normal and PVL animals. Control, PVL, CBDL, TAA-treated, and ET-1-infused PVL animals had ET-1 and TNF-alpha levels measured and underwent molecular and physiological evaluation for HPS. HPS developed only in biliary cirrhosis in association with increased plasma ET-1 and TNF-alpha levels and the development of established molecular changes in the pulmonary microvasculature. In contrast, PVL did not increase ET-1 or TNF-alpha levels and TAA treatment increased TNF-alpha levels alone, and neither resulted in the full development of molecular or physiological changes of HPS despite portal pressure increases similar to those after CBDL. Exogenous ET-1 increased TNF-alpha levels and triggered HPS after PVL. Combination of ET-1 and TNF-alpha overproduction is unique to biliary cirrhosis and associated with experimental HPS. ET-1 infusion increases TNF-alpha levels and triggers HPS in prehepatic portal hypertension. ET-1 and TNF-alpha interact to trigger pulmonary microvascular changes in experimental HPS.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

ET-1 and TNF-α in HPS: analysis in prehepatic portal hypertension and biliary and nonbiliary cirrhosis in rats

Luo¹,

Liu²,

Tang³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

103

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“…26,40,[46][47][48] Src kinases are activated by a variety of growth factors. Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor stimulate Src activation in avian endothelial cells, and sE-selectin and VEGF mediate angiogenesis via Src family tyrosine kinases.…”

Section: Discussionmentioning

confidence: 99%

Migration inhibitory factor up-regulates vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 via Src, PI3 kinase, and NFκB

Amin

Haas

Zhu

et al. 2006

Blood

131

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IntroductionMigration inhibitory factor (MIF) is a pleotropic cytokine which plays a pivotal role in inflammatory and immune-mediated diseases such as rheumatoid arthritis (RA) and atherosclerosis. MIF is secreted by T lymphocytes and macrophages on lipopolysaccharide (LPS) exposure and induces secretion of tumor necrosis factor-␣ (TNF-␣) by mouse macrophages. 1,2 In RA, MIF is highly expressed in macrophages, endothelial cells, synovial tissue (ST) fibroblasts, serum, and synovial fluids. 1,2 MIF stimulates macrophage release of proinflammatory cytokines such as TNF-␣, interleukin 1 ␤ (IL-1␤), 4 MIF up-regulates IL-1␤, matrix metalloproteinases (MMPs) MMP-1, MMP-3, MMP-9, and MMP-13 in RA ST fibroblasts. 5,6 In rodent arthritis models, administration of anti-MIF antibody ameliorates arthritis with profound inhibition of clinical and histologic features of disease. [7][8][9] Anti-MIF treatment ameliorates acute encephalomyelitis and experimental autoimmune myocarditis in mice. 10,11 These studies show a key role of MIF in the pathogenesis of immunologic and inflammatory diseases.We have shown that MIF is a potent angiogenic factor. 12 Anti-MIF inhibits tumor growth and tumor-associated angiogenesis, and MIF is a required factor for tumor-initiated endothelial cell proliferation and tumor neovascularization. 13,14 Vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) in soluble forms (sVCAM-1 and sICAM-1, respectively) are potent angiogenic mediators, and RA synovial fluid-induced angiogenesis is blocked by anti-VCAM-1. 15,16 MIF is found in human vascular endothelial cells, which have been considered to play a pivotal role in systemic inflammatory and immunologic diseases by producing cytokines and growth factors. 17 Adhesion of inflammatory cells to vascular endothelium is the initial step in leukocyte recruitment and is mediated by a number of cell adhesion molecules such as ICAM-1, VCAM-1, E-, P-, and L-selectin, as well as integrins. MIF up-regulates ICAM-1 on endothelial cells. 18 Rat kidney VCAM-1 and ICAM-1 expression are decreased by anti-MIF treatment, blocking the development of glomerulonephritis. 19 Similarly, anti-MIF prevents VCAM-1 up-regulation on endothelial cells and improves acute encephalomyelitis in mice. 11 Cell adhesion molecules mediate and amplify the inflammatory response by allowing the ingress of leukocytes into diseased tissues. 20-22 VCAM-1 and ICAM-1 may be used as a reliable measure of the extent of atherosclerotic progression, and focal expression of adhesion molecules is consistently found in atherosclerotic plaques in humans. [22][23][24] The most compelling data for the necessity of adhesion molecules in the development of atherosclerotic plaques came from a report indicating that mice deficient in adhesion molecules are protected against atherosclerosis when fed an atherogenic diet. 25 Those studies support the role of adhesion molecules in immune-mediated diseases. For personal use only. on May 11, 2018. by guest www.bloodjournal.org From ...

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“…HMVECs stimulated with sEselectin showed phosphorylation of a number of proteins corresponding to molecular weights of 140 to 150, 130 to 140, 55 to 65, and 30 to 40 kDa (data not shown). As the predominant band obtained using anti-phosphotyrosine antibody was observed in the molecular-weight range of Src kinase, and the Src family kinases are known to play an important role in a number of physiologic functions including monocyte adherence to endothelial cells, 28 endothelial cell differentiation, 29 endothelial cell survival, 30 and endothelial cell proliferation and angiogenesis, 1 we examined the role of Src kinase in sE-selectin-stimulated HMVECs. sE-selectin induced a marked increase in HMVEC Src kinase phosphorylation, which was substantially inhibited by PP2 or by transfecting the HMVECs with Src antisense ODNs, thus indicating that Src may be an important mediator in sE-selectin-induced signaling in HMVECs.…”

Section: Discussionmentioning

confidence: 99%

Src and phosphatidylinositol 3–kinase mediate soluble E-selectin–induced angiogenesis

Kumar

Amin

Harlow

et al. 2003

Blood

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Angiogenesis plays an important role in a variety of pathophysiologic processes, including tumor growth and rheumatoid arthritis. We have previously shown that soluble E-selectin (sE-selectin) is an important angiogenic mediator. However, the mechanism by which sE-selectin mediates angiogenesis is still unknown. In this study, we show that sE-selectin is a potent mediator of human dermal microvascular endothelial cell (HMVEC) chemotaxis, which is predominantly mediated through the Src and the phosphatidylino-

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Modulation of monocyte adherence to endothelial cells by endothelin-1 involvement of Src (p60src) and JAK1-like kinases

Abstract: These data suggest an association between activation of p60SRC and JAK1-like kinases and monocyte adherence in response to ET-1. ET-1-induced monocyte adherence is upregulated by ET B receptor antagonist, suggesting a negative feedback on cell adhesion through this receptor.

Cited by 13 publications

References 32 publications

ET-1 and TNF-α in HPS: analysis in prehepatic portal hypertension and biliary and nonbiliary cirrhosis in rats

ET-1 and TNF-α in HPS: analysis in prehepatic portal hypertension and biliary and nonbiliary cirrhosis in rats

Migration inhibitory factor up-regulates vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 via Src, PI3 kinase, and NFκB

Src and phosphatidylinositol 3–kinase mediate soluble E-selectin–induced angiogenesis

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