High Glucose–Induced Alterations in Subendothelial Matrix Perlecan Leads to Increased Monocyte Binding

Vogl-Willis, Catherine A; Edwards, Iris J.

doi:10.1161/01.atv.0000126375.60073.74

Cited by 23 publications

(14 citation statements)

References 45 publications

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“…These findings not only expand our understanding of the initial steps of atherosclerosis but also provide a potential avenue for therapeutic intervention on atherosclerotic diseases in humans. Monocyte adhesion to extracellular matrix proteins on endothelial surface has been considered as the major early step in the initiation of atherosclerosis [Huo et al, 2000;Vogl-Willis and Edwards, 2004]. For example, both soluble plasma and insoluble cellular fibronectin, as a known ligand to integrin receptor (a 5 b 1 ) of monocytes [Schmidt and Kao, 2007], can activate the integrin signaling pathway that leads to cell adhesion, cell migration, and morphogenesis [Miyamoto et al, 1998].…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone inhibits monocyte/macrophage adhesion through de novo adiponectin production in human monocytes

Tsai

Chen

et al. 2010

J of Cellular Biochemistry

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Rosiglitazone (RSG) has a variety of actions on both insulin sensitization and anti-atherogenic effects. The molecular effect of RSG on monocyte/macrophage function in terms of de novo synthesis of adiponectin is not fully understood. Here, we examined the regulation of adiponectin expression in human monocytes/macrophages by RSG and its function on monocyte adhesion during initiation of atherosclerosis. Adiponectin expression in monocytes and macrophages was studied by RT-PCR, quantitative real-time PCR, Western blot, and immunocytochemistry. Signal transduction and adhesion molecules were studied in order to describe the function of de novo synthesized adiponectin in monocyte adhesion. Adiponectin was expressed and upregulated during monocyte differentiation. The expression of adiponectin was enhanced, albeit at a much lesser degree, by a peroxisome proliferator-activated receptor gamma (PPAR gamma) agonist RSG, which was similar to what was found in adipocytes. Monocyte adhesion was remarkably reduced when the cells were treated with RSG for 12 h. This inhibitory effect of RSG was abolished by specific anti-adiponectin antibodies but not by non-immune immunoglobulin G in a serum-free condition. Adiponectin-induced suppression on monocyte adhesion was inhibited by a selective AMP-activated protein kinase (AMPK) inhibitor compound C. The reduced expression and/or function of adhesion molecule integrins may underlie the mechanism contributing to reduced monocyte adhesion upon AMPK activation. Our data suggest that the inhibitory effect of RSG on monocyte adhesion might be at least in part through de novo adiponectin expression and activation of an AMPK-dependent pathway, which might play an important role in atherogenesis.

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Section: Discussionmentioning

confidence: 99%

Rosiglitazone inhibits monocyte/macrophage adhesion through de novo adiponectin production in human monocytes

Tsai

Chen

et al. 2010

J of Cellular Biochemistry

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“…This suggests that whereas the local environment might have caused ECs to change BM deposition in vivo, a change in EC phenotype was not imprinted or maintained in a uniform culture system. Indeed, when ECs were cultured in high glucose, to model diabetes, the adhesion of monocytes to the BM was modified [94], an effect attributable to modification of the proteoglycans. This study supports the concept that endothelial conditioning can modulate the BM constitution, leading to functional changes, which impact on the process of leukocyte recruitment.…”

Section: Modification Of Bm Structure In Diseasementioning

confidence: 99%

Tissue stroma as a regulator of leukocyte recruitment in inflammation

McGettrick

Butler

Buckley

et al. 2012

Journal of Leukocyte Biology

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The stromal milieu (cellular and matrix components) helps establish tissue "address-codes" that direct leukocyte behavior in inflamed tissue. Coordinated interactions among the stroma, leukocytes, and ECs dictate which leukocytes are recruited, whether they are retained within the inflamed site, and how long they survive. Herein, we discuss how the stromal milieu influences the leukocyte recruitment cascade. Moreover, we explore how corruption of the stromal phenotype in chronic inflammatory diseases contributes to undesired, continuous recruitment of leukocytes. Emerging complex, multicellular, multilayered (co-)culture models are now addressing the molecular circuitry involved in regulating stromal organization during inflammation. Understanding context-specific changes in pro- or anti-inflammatory agents derived from the stroma, such as IL-6 (and its cofactors), is important for the generation of therapeutic strategies that restore the balance between recruitment and clearance of the inflammatory infiltrate in chronic disease.

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“…One is based on studies demonstrating anti-proliferative effects of HS on arterial smooth muscle cells [25]. HSPG are produced by arterial smooth muscle cells but the major contributors of arterial HS are endothelial cells which secrete the basement membrane HSPG, perlecan, into the sub-endothelial matrix (Figure 5 and [46]). We have recently shown that in cultured human and bovine aortic endothelial cells, high glucose exposure results in a structural modification of perlecan that is consistent with the loss of an HS GAG chain [46,47].…”

Section: Discussionmentioning

confidence: 99%

Arterial heparan sulfate is negatively associated with hyperglycemia and atherosclerosis in diabetic monkeys

Edwards

Wagner

Vogl-Willis

et al. 2004

Cardiovasc Diabetol

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Background: Arterial proteoglycans are implicated in the pathogenesis of atherosclerosis by their ability to trap plasma lipoproteins in the arterial wall and by their influence on cellular migration, adhesion and proliferation. In addition, data have suggested an anti-atherogenic role for heparan sulfate proteoglycans and a pro-atherogenic role for dermatan sulfate proteoglycans. Using a nonhuman primate model for human diabetes, studies examined diabetes-induced changes in arterial proteoglycans that may increase susceptibility to atherosclerosis.

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High Glucose–Induced Alterations in Subendothelial Matrix Perlecan Leads to Increased Monocyte Binding

Cited by 23 publications

References 45 publications

Rosiglitazone inhibits monocyte/macrophage adhesion through de novo adiponectin production in human monocytes

Rosiglitazone inhibits monocyte/macrophage adhesion through de novo adiponectin production in human monocytes

Tissue stroma as a regulator of leukocyte recruitment in inflammation

Arterial heparan sulfate is negatively associated with hyperglycemia and atherosclerosis in diabetic monkeys

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