Angiopoietin-1 Reduces VEGF-Stimulated Leukocyte Adhesion to Endothelial Cells by Reducing ICAM-1, VCAM-1, and E-Selectin Expression

Kim, Injune; Moon, Sang-Ok; Park, Sung Kwang; Chae, Soo Wan; Koh, Gou Young

doi:10.1161/hh1801.097034

Cited by 316 publications

(241 citation statements)

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“…It is also possible that the plasma exudates may readily pass the inflamed mucosa and reach the airway lumen through leaky epithelium, thus compromising epithelial integrity and reducing ciliary function and mucus clearance (Foster et al, 1982;Persson, 1996). Although some investigators have described a role for Ang1 in promoting chemotaxis and migration of leukocytes in vitro (Feistritzer et al, 2004;Lemieux et al, 2005), Ang1 has also been shown to reduce leukocyte trafficking in inflammation through the modulation of various inflammatory mediators (Kim et al, 2001;Pizurki et al, 2003;Witzenbichler et al, 2005). Th2 cytokines, adhesion molecules, chemokines, and VEGF play a crucial role in the chemotactic responses for leukocytes, including eosinophils (Wegner et al, 1990;Montefort and Holgate, 1991;Moser et al, 1992;Seder et al, 1992;Foster et al, 1996;Pawankar et al, 1997;Dabbagh et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…Ang1-and Tie2-deficient mice have similar phenotypes characterized by embryonic lethality with severe vascular remodeling defects, insufficient vessel stabilization, and perturbed vascular maturation (Sato et al, 1993;Suri et al, 1996). In addition, Ang1 can counteract VEGF-induced side effects (Thurston et al, 2000;Kim et al, 2001) while having an additive effect on vessel formation (Chae et al, 2000;Thurston et al, 2000). These observations have suggested that Ang1 has potential therapeutic applications in inducing angiogenesis, enhancing endothelial cell survival, and preventing vascular leakage.…”

Section: Introductionmentioning

confidence: 99%

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Blockade of airway inflammation and hyper-responsiveness by an angiopoietin-1 variant, COMP-Ang1

Lee

Lee²,

Kim³

et al. 2007

Exp Mol Med

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Inflammation of the asthmatic airway is usually accompanied by increased vascular permeability and plasma exudation. Angiopoietin-1 (Ang1) has potential therapeutic applications in preventing vascular leakage. Recently, we developed a soluble, stable, and potent Ang1 variant, COMP-Ang1. COMP-Ang1 is more potent than native Ang1 in phosphorylating the tyrosine kinase with immunoglobulin and epidermal growth factor homology domain 2 receptor in lung endothelial cells. We have used a mouse model for allergic airway disease to determine effects of COMP-Ang1 on allergen-induced bronchial inflammation and airway hyper-responsiveness. These mice develop the following typical pathophysiological features of allergic airway disease in the lungs: increased numbers of inflammatory cells of the airways, airway hyper-responsiveness, increased levels of Th2 cell cytokines (IL-4, IL-5, and IL-13), adhesion molecules (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1), and chemokines (eotaxin and RANTES), and increased vascular permeability. Intravenous administration of COMP-Ang1 reduced bronchial inflammation and airway hyper-responsiveness. In addition, the increased plasma extravasation in allergic airway disease was significantly reduced by the administration of COMP-Ang1. These results suggest that COMP-Ang1 attenuates airway inflammation and hyper-responsiveness, prevents vascular leakage, and may be used as a therapeutic agent in allergic airway disease.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Blockade of airway inflammation and hyper-responsiveness by an angiopoietin-1 variant, COMP-Ang1

Lee

Lee²,

Kim³

et al. 2007

Exp Mol Med

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“…VEGF-A stimulation of human umbilical vein endothelial cells increases the expression of adhesion molecules, such as ICAM-1, VCAM-1, and selectins (68,75). This induction of adhesion molecule expression increases in vitro leukocyte adhesion under static conditions, which occurs through the activation of VEGF-R2 (75,76). Importantly, we have recently reported that VEGF-A stimulates increased ICAM-1 expression on distal colon microvascular endothelium, which facilitates neutrophil and T cell adhesion in a CD18-dependent manner (55).…”

Section: Angiogenic Mediators In Ibd and Experimental Colitismentioning

confidence: 99%

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Chidlow

Shukla²,

Grisham³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

144

114

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Chidlow JH Jr, Shukla D, Grisham MB, Kevil CG. Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues. Am J Physiol Gastrointest Liver Physiol 293: G5-G18, 2007. First published April 26, 2007; doi:10.1152/ajpgi.00107.2007.-Angiogenesis is now understood to play a major role in the pathology of chronic inflammatory diseases and is indicated to exacerbate disease pathology. Recent evidence shows that angiogenesis is crucial during inflammatory bowel disease (IBD) and in experimental models of colitis. Examination of the relationship between angiogenesis and inflammation in experimental colitis shows that initiating factors for these responses simultaneously increase as disease progresses and correlate in magnitude. Recent studies show that inhibition of the inflammatory response attenuates angiogenesis to a similar degree and, importantly, that inhibition of angiogenesis does the same to inflammation. Recent data provide evidence that differential regulation of the angiogenic mediators involved in IBD-associated chronic inflammation is the root of this pathological angiogenesis. Many factors are involved in this phenomenon, including growth factors/cytokines, chemokines, adhesion molecules, integrins, matrix-associated molecules, and signaling targets. These factors are produced by various vascular, inflammatory, and immune cell types that are involved in IBD pathology. Moreover, recent studies provide evidence that antiangiogenic therapy is a novel and effective approach for IBD treatment. Here we review the role of pathological angiogenesis during IBD and experimental colitis and discuss the therapeutic avenues this recent knowledge has revealed. inflammation; T cells; growth factors; adhesion molecules; antiangiogenesis ANGIOGENESIS PLAYS AN IMPORTANT role in many chronic inflammatory diseases including but not limited to diabetic retinopathy, atherosclerosis, rheumatoid arthritis, hypercholesterolemia, and psoriasis. It has been suggested that the angiogenic components of these diseases contribute to and exacerbate disease conditions (26, 31). Recent findings, both clinical and experimental, indicate that angiogenesis also plays a crucial role in the inflammatory bowel diseases (IBD), consisting of Crohn's disease (CD) and ulcerative colitis (UC) (31,37,58,131,155). Development of new vasculature during chronic inflammation may play a negative "pathological" role by contributing to increased inflammatory responses due to dysfunctional new vessel architecture and increases in the recruitment of inflammatory cell types. Importantly, recent data have shown that angiogenic inhibition during chronic inflammatory diseases attenuates further inflammation and disease pathology (31, 37, 51). As such, expanding our knowledge of how pathological angiogenesis occurs during IBD will further our ability to treat patients with these diseases. IBD PathogenesisCD and UC are idiopathic inflammatory disorders of the intestine and/or colon in which patients suffer from rectal bleeding, severe...

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“…1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 16 angiopoietin-1 (Ang1) has both angiogenic and anti-inflammatory properties [55,56,57]. For example, binding of Ang1 to Tie2 inhibits the NF-B-dependent expression of adhesion molecules, decreases the permeability of endothelial monolayers and impedes TNF-induced transmigration of leukocytes [58,59]. ABIN-2 was found to interact with the cytoplasmic tail of Tie2 via a domain encompassing AHD1.…”

Section: Abin-2mentioning

confidence: 99%

ABINs: A20 binding inhibitors of NF-κB and apoptosis signaling

Verstrepen¹,

Carpentier²,

Verhelst³

et al. 2009

Biochemical Pharmacology

161

126

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ABINs have been described as three different proteins (ABIN-1, ABIN-2, that bind the ubiquitin-editing nuclear factor-B (NF-B) inhibitor protein A20 and which show limited sequence homology. Overexpression of ABINs inhibits NF-B activation by tumor necrosis factor (TNF) and several other stimuli. Similar to A20, ABIN-1 and ABIN-3 expression is NF-B dependent, implicating a potential role for the A20/ABIN complex in the

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Angiopoietin-1 Reduces VEGF-Stimulated Leukocyte Adhesion to Endothelial Cells by Reducing ICAM-1, VCAM-1, and E-Selectin Expression

Cited by 316 publications

References 11 publications

Blockade of airway inflammation and hyper-responsiveness by an angiopoietin-1 variant, COMP-Ang1

Blockade of airway inflammation and hyper-responsiveness by an angiopoietin-1 variant, COMP-Ang1

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

ABINs: A20 binding inhibitors of NF-κB and apoptosis signaling

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