A Novel Function for a Glucose Analog of Blood Group H Antigen as a Mediator of Leukocyte-Endothelial Adhesion via Intracellular Adhesion Molecule 1

Zhu, Kui; Amin, M. Asif; Kim, Michael J.; Katschke, Kenneth J.; Park, Christy C.; Koch, Alisa E.

doi:10.1074/jbc.m213052200

Cited by 32 publications

(44 citation statements)

References 29 publications

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“…Furthermore, H type 2 antigens mediate leukocyte-endothelial adhesion through intracellular adhesion molecule, suggesting that they are involved in the progression of inflammation (Zhu et al 2003). On the other hand, A type 3 determinants seemed to be carried on vWF in endothelial cells in inflamed tissues (Figure 5), suggesting that aberrantly expressed A type 3 antigens play a role in blood coagulation.…”

Section: Discussionmentioning

confidence: 99%

Aberrant Expression of Histo-blood Group A Type 3 Antigens in Vascular Endothelial Cells in Inflammatory Sites

Nosaka

Ishida

Tanaka

et al. 2007

J Histochem Cytochem.

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Histo-blood group ABH antigens are widely distributed in human tissues. The epitopes of ABH antigens are carried by at least four different peripheral core isotypes of internal carbohydrate backbones (type 1–4). Each type of ABH antigen is expressed tissue specifically, and aberrant expression of ABH antigens is often observed during oncogenesis. We immunohistochemically examined the expression of A type 3 antigens in wounded and diseased skin tissues (A and AB blood groups). In uninjured skin, the expression of A type 3 antigens was restricted to the eccrine sweat gland. In addition to the sweat glands, A type 3 antigens were found in vascular endothelial cells of the wound sites. The extent of A type 3 antigens expression related to postinfliction intervals. A significantly higher expression rate of A type 3 antigens in endothelial cells was also observed in diseased skin, suggesting that inflammation might induce A type 3 antigen expression in endothelial cells. Double-color immunofluorescence staining of the specimens showed that von Willebrand factor (vWF) was a core-protein of A type 3 determinants aberrantly expressed in endothelial cells in inflamed tissues, suggesting that aberrant expression of A type 3 antigens is involved in stabilization of vWF in inflammation.

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Section: Discussionmentioning

confidence: 99%

Aberrant Expression of Histo-blood Group A Type 3 Antigens in Vascular Endothelial Cells in Inflammatory Sites

Nosaka

Ishida

Tanaka

et al. 2007

J Histochem Cytochem.

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“…Cell lysis and immunoblotting were performed as described previously (37,38). Briefly, freshly isolated human MNCs were incubated in 6-well plates for at least 12 hours (2 ϫ 10 6 /well) in serum-free RPMI 1640 prior to stimulation with 10 nM CXCL16 for various time periods.…”

Section: Methodsmentioning

confidence: 99%

CXCL16‐mediated cell recruitment to rheumatoid arthritis synovial tissue and murine lymph nodes is dependent upon the MAPK pathway

Ruth¹,

Haas²,

Park³

et al. 2006

Arthritis & Rheumatism

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107

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Objective. Rheumatoid arthritis (RA) is characterized by profound mononuclear cell (MNC) recruitment into synovial tissue (ST), thought to be due in part to tumor necrosis factor ␣ (TNF␣), a therapeutic target for RA. Although chemokines may also be involved, the mechanisms remain unclear. We undertook this study to examine the participation of CXCL16, a novel chemokine, in recruitment of MNCs to RA ST in vivo and to determine the signal transduction pathways mediating this process. Conclusion. Taken together, these results point to a unique role for CXCL16 as a premier MNC recruiter in RA and suggest additional therapeutic possibilities, targeting CXCL16, its receptor, or its signaling pathways.

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“…26,36,37 It is a downstream target of Src, PI3K, p38, and Jak2 and a key transcription factor regulating inflammation. 28,38,39 In this study, we demonstrate a direct effect of rhMIF in up-regulating VCAM-1 and ICAM-1 in human peripheral blood (PB) monocytes (MNs) using cell-surface enzyme-linked immunosorbent assays (ELISAs). We report the role of Src, PI3K, p38, and NFB in up-regulating these adhesion molecules.…”

mentioning

confidence: 99%

“…on May 11, 2018. by guest www.bloodjournal.org From Cell adhesion molecules may be up-regulated via different protein tyrosine kinases such as Src, phosphatidylinositol 3 kinase (PI3K), Erk1/2, Jak2, Stat3, and NFB. [26][27][28][29] We and others have shown that vascular endothelial growth factor and sE-selectin mediate angiogenesis via Src kinases. 30,31 Src family kinases mediate the multistep process of leukocyte adhesion, migration, and accumulation at inflammatory sites by the interaction of a number of adhesion molecules on leukocytes and endothelial cells.…”

mentioning

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

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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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A Novel Function for a Glucose Analog of Blood Group H Antigen as a Mediator of Leukocyte-Endothelial Adhesion via Intracellular Adhesion Molecule 1

Cited by 32 publications

References 29 publications

Aberrant Expression of Histo-blood Group A Type 3 Antigens in Vascular Endothelial Cells in Inflammatory Sites

Aberrant Expression of Histo-blood Group A Type 3 Antigens in Vascular Endothelial Cells in Inflammatory Sites

CXCL16‐mediated cell recruitment to rheumatoid arthritis synovial tissue and murine lymph nodes is dependent upon the MAPK pathway

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

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