Participation of high glucose concentrations in neutrophil adhesion and surface expression of adhesion molecules on cultured human endothelial cells

Omi, Hitoshi; Okayama, Naotsuka; Shimizu, Manabu; Okouchi, Masahiro; Ito, Shigenori; Fukutomi, Tatsuya; Itoh, Makoto

doi:10.1016/s1056-8727(01)00163-5

Cited by 82 publications

(59 citation statements)

References 45 publications

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“…The results obtained with the SIEFED technique emphasized the importance of measuring the active part of MPO, which is the real witness of the oxidant potential of the enzyme that is not taken into consideration by a classical ELISA. Indeed, the presence of free active MPO increases the risk of cytotoxicity, as the enzyme is taken up by cells or binds on the cell surface with an in situ production of oxidant species [34,35], which are involved in chlorination and nitration of proteins [2,6], and surely contribute to the pathogenesis of the disease [2,6] or to the modulation of the inflammation reaction [36].…”

Section: Discussionmentioning

confidence: 99%

A new easy method for specific measurement of active myeloperoxidase in human biological fluids and tissue extracts

Franck

Kohnen

Boudjeltia³

et al. 2009

Talanta

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a b s t r a c tThe SIEFED ("Specific Immunological Extraction Followed by Enzymatic Detection") method already developed for the specific detection of the activity of equine myeloperoxidase (MPO) was adapted for the specific measurement of active human MPO in biological fluids or tissue extracts. The method consists of the extraction of MPO from aqueous solutions by immobilized anti-MPO antibodies followed by a washing (to eliminate the extraction medium and the biological fluid with their possible interfering molecules) and the measurement of the activity of MPO with a detection system containing a fluorogenic substrate, H 2 O 2 and nitrite ions as reaction enhancer. The SIEFED was applied to study active MPO in human biological fluids (plasma, bronchoalveolar lavage fluid and supernatant from carotids extracts). The SIEFED for human MPO has a sensitivity limit of 0.080 mU/mL and showed good precision with intra-and inter-assay coefficients of variation below 10 and 20% respectively within a broad range of MPO activities establish from 0.156 to 473 mU/mL. The SIEFED for human MPO will be useful for the specific detection of active MPO in complex fluids and can be complementary to an ELISA to determine an active/total MPO ratio in healthy volunteers and patients especially in case of chronic or acute inflammatory diseases.

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Section: Discussionmentioning

confidence: 99%

A new easy method for specific measurement of active myeloperoxidase in human biological fluids and tissue extracts

Franck

Kohnen

Boudjeltia³

et al. 2009

Talanta

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“…104 In endothelial cells cultured in high-glucose concentrations, neutrophil adherence and expression of ICAM-1, E-selectin, and P-selectin are increased, but this can be prevented by incubation with PKC inhibitors. 105 High-glucose concentrations was shown to increase NFB activation and VCAM-1 expression in endothelial cell culture, and these events were inhibited by a selective PKC␤2 inhibitor. 106 However, VCAM-1 induction stimulated by thrombin has been shown to be mediated by PKC␦ and PKC through binding of NFB and GATA-2, respectively, to the VCAM-1 promotor.…”

Section: Induction Of Adhesion Moleculesmentioning

confidence: 98%

Proatherosclerotic Mechanisms Involving Protein Kinase C in Diabetes and Insulin Resistance

Rask‐Madsen

King

2005

ATVB

157

128

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Abstract-In diabetes and insulin resistance, activation of protein kinase C (PKC) in vascular cells may be a key linkbetween elevated plasma and tissue concentrations of glucose and nonesterified fatty acids and abnormal vascular cell signaling. Initial studies of PKC activation in diabetes focused on microvascular complications, but increasing evidence supports that PKC plays a role in several mechanisms promoting atherosclerosis. This review explains how PKC is thought to be activated in diabetes and insulin resistance through de novo synthesis of diacylglycerol. Furthermore, the review summarizes studies that implicate PKC in promoting proatherogenic mechanisms or inhibiting antiatherogenic mechanisms, including studies of endothelial dysfunction; gene induction and activation of vascular NAD(P)H oxidase; endothelial nitric oxide synthase expression and function; endothelin-1 expression; growth, migration, and apoptosis of vascular smooth muscle cells; induction of adhesion molecules; and oxidized low-density lipoprotein uptake by monocyte-derived macrophages.

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“…112 This is supported by the observation that although DR is a microvascular disease microangiopathy does not seem to have a major pathogenic role in the cerebral complications of diabetes and the blood--brain barrier is not as susceptible to hyperglycaemia as the retinal microvasculature. 113 It has been reported that hyperglycaemia can stimulate both NF-κB-and PKC-dependent pathways thus upregulating endothelial adhesion molecules, such as ICAM-1 (CD54) or E-Selectin (CD62E), [114][115][116] vascular cell adhesion molecule-1 (CD106), 117 and platelet endothelial cell adhesion molecule (CD31), in ECs. ICAM-1 upregulation is thought to be VEGF dependent, whereas P-and E-Selectin are not.…”

Section: Scientific Basismentioning

confidence: 99%

A review of therapies for diabetic macular oedema and rationale for combination therapy

Amoaku

Saker

Stewart

2015

Eye

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Diabetic macular oedema (DMO) is responsible for significant visual impairment in diabetic patients. The primary cause of DMO is fluid leakage resulting from increased vascular permeability through contributory anatomical and biochemical changes. These include endothelial cell (EC) death or dysfunction, pericyte loss or dysfunction, thickened basement membrane, loss or dysfunction of glial cells, and loss/change of EC Glycocalyx. The molecular changes include increased reactive oxygen species, pro-inflammatory changes: advanced glycation end products, intracellular adhesion molecule-1, Complement 5-9 deposition and cytokines, which result in increased paracellular permeability, tight junction disruption, and increased transcellular permeability. Laser photocoagulation has been the mainstay of treatment until recently when pharmacological treatments were introduced. The current treatments for DMO target reducing vascular leak in the macula once it has occurred, they do not attempt to treat the underlying pathology. These pharmacological treatments are aimed at antagonising vascular endothelial growth factor (VEGF) or non-VEGF inflammatory pathways, and include intravitreal injections of anti-VEGFs (ranibizumab, aflibercept or bevacizumab) or steroids (fluocinolone, dexamethasone or triamcinolone) as single therapies. The available evidence suggests that each individual treatment modality in DMO does not result in a completely dry macula in most cases. The ideal treatment for DMO should improve vision and improve morphological changes in the macular (eg, reduce macular oedema) for a significant duration, reduced adverse events, reduced treatment burden and costs, and be well tolerated by patients. This review evaluates the individual treatments available as monotherapies, and discusses the rationale and potential for combination therapy in DMO.

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Participation of high glucose concentrations in neutrophil adhesion and surface expression of adhesion molecules on cultured human endothelial cells

Cited by 82 publications

References 45 publications

A new easy method for specific measurement of active myeloperoxidase in human biological fluids and tissue extracts

A new easy method for specific measurement of active myeloperoxidase in human biological fluids and tissue extracts

Proatherosclerotic Mechanisms Involving Protein Kinase C in Diabetes and Insulin Resistance

A review of therapies for diabetic macular oedema and rationale for combination therapy

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