Advanced glycosylation end products induced tissue factor expression in human monocyte-like U937 cells and increased tissue factor expression in monocytes from diabetic patients

Ichikawa, Kojiro; Yoshinari, Mototaka; Iwase, Masanori; Wakisaka, Masanori; Doi, Yasufumi; Iino, Kenzo; Yamamoto, Masato; Fujishima, Masatoshi

doi:10.1016/s0021-9150(97)00221-9

Cited by 64 publications

(46 citation statements)

References 33 publications

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“…Ligand Preparation and Radiolabeling-AGE-BSA was prepared as described previously (19). 600 mg of BSA was incubated with 50 mM glucose 6-phosphate in 10 ml of sterile sodium phosphate buffer or phosphate-buffered saline (PBS) for 10 weeks at 37°C and dialyzed overnight against PBS.…”

Section: Methodsmentioning

confidence: 99%

FEEL-1 and FEEL-2 Are Endocytic Receptors for Advanced Glycation End Products

Tamura

Adachi

Osuga

et al. 2003

Journal of Biological Chemistry

185

136

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Section: Methodsmentioning

confidence: 99%

FEEL-1 and FEEL-2 Are Endocytic Receptors for Advanced Glycation End Products

Tamura

Adachi

Osuga

et al. 2003

Journal of Biological Chemistry

185

136

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“…82 AGEs also alter cellular coagulant properties, partly via the monocyte-produced procoagulant, tissue factor, and decreased expression of the endothelial anticoagulant cofactor, thrombomodulin. 23,71,80,83,84 …”

Section: Age and The Macrophagementioning

confidence: 99%

Advanced Glycation End Products

et al. 2006

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Abstract-Advanced glycation end products (AGEs) are proteins or lipids that become glycated after exposure to sugars.AGEs are prevalent in the diabetic vasculature and contribute to the development of atherosclerosis. The presence and accumulation of AGEs in many different cell types affect extracellular and intracellular structure and function. AGEs contribute to a variety of microvascular and macrovascular complications through the formation of cross-links between molecules in the basement membrane of the extracellular matrix and by engaging the receptor for advanced glycation end products (RAGE). Activation of RAGE by AGEs causes upregulation of the transcription factor nuclear factor-B and its target genes. Soluble AGEs activate monocytes, and AGEs in the basement membrane inhibit monocyte migration. AGE-bound RAGE increases endothelial permeability to macromolecules. AGEs block nitric oxide activity in the endothelium and cause the production of reactive oxygen species.

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“…Therefore, heterogeneity in aminophospholipid content could account for the differences observed in the procoagulant phenotype of microparticles released in the two diabetic populations. In addition, several studies have described changes of tissue factor pathway in diabetes and their involvement in the vascular complications (36). Accordingly, another procoagulant mechanism could result from tissue factor expression by microparticles.…”

Section: Diabetes Vol 51 September 2002mentioning

confidence: 99%

Type 1 And Type 2 Diabetic Patients Display Different Patterns of Cellular Microparticles

Sabatier

Darmon

Hugel³

et al. 2002

Diabetes

355

243

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The development of vasculopathies in diabetes involves multifactorial processes including pathological activation of vascular cells. Release of microparticles by activated cells has been reported in diseases associated with thrombotic risk, but few data are available in diabetes. The aim of the present work was to explore the number and the procoagulant activity of cell-derived microparticles in type 1 and 2 diabetic patients. Compared with age-matched control subjects, type 1 diabetic patients presented significantly higher numbers of platelet and endothelial microparticles (PMP and EMP), total annexin V-positive blood cell microparticles (TMP), and increased levels of TMP-associated procoagulant activity. In type 2 diabetic patients, only TMP levels were significantly higher without concomitant increase of their procoagulant activity. Interestingly, in type 1 diabetic patients, TMP procoagulant activity was correlated with HbA 1c , suggesting that procoagulant activity is associated with glucose imbalance. These results showed that a wide vesiculation process, resulting from activation or apoptosis of several cell types, occurs in diabetes. However, diabetic patients differ by the procoagulant activity and the cellular origin of microparticles. In type 1 diabetic patients, TMP-procoagulant activity could be involved in vascular complications. Moreover, its correlation with HbA 1c reinforces the importance of an optimal glycemic control in type 1 diabetes.

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Advanced glycosylation end products induced tissue factor expression in human monocyte-like U937 cells and increased tissue factor expression in monocytes from diabetic patients

Cited by 64 publications

References 33 publications

FEEL-1 and FEEL-2 Are Endocytic Receptors for Advanced Glycation End Products

FEEL-1 and FEEL-2 Are Endocytic Receptors for Advanced Glycation End Products

Advanced Glycation End Products

Type 1 And Type 2 Diabetic Patients Display Different Patterns of Cellular Microparticles

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