Shear stress-stimulated endothelial cells induce smooth muscle cell chemotaxis via platelet-derived growth factor-BB and interleukin-1α

Dardik, Alan; Yamashita, Atsuo; Aziz, Faisal; Asada, Hidenori; Sumpio, Bauer E.

doi:10.1016/j.jvs.2004.11.016

Cited by 86 publications

(54 citation statements)

References 63 publications

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“…This is because PDGF expression is sensitive to changes in flow, and PDGF is thought to play a major role in SMC migration during pathologic arterial remodeling [19,20]. Rat A-10 cells exposed to BMP4 exhibited less PDGF-induced migration in a dose dependent manner.…”

Section: Bmp Receptor Activation Inhibits Smc Migrationmentioning

confidence: 99%

Endothelial Bmp4 Is Induced During Arterial Remodeling: Effects on Smooth Muscle Cell Migration and Proliferation

Corriere

Rogers

Eliason

et al. 2008

Journal of Surgical Research

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Background-Bone morphogenetic proteins (BMPs) are members of the TGF-β superfamily of proteins that have multiple functional roles in mammalian development. A role for BMP4 in adult vascular remodeling has recently been suggested. We evaluated the expression of Bmp4 during neointimal lesion development in vivo. We then assessed the role BMP4 signaling on SMC function during neointimal lesion development.

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Section: Bmp Receptor Activation Inhibits Smc Migrationmentioning

confidence: 99%

Endothelial Bmp4 Is Induced During Arterial Remodeling: Effects on Smooth Muscle Cell Migration and Proliferation

Corriere

Rogers

Eliason

et al. 2008

Journal of Surgical Research

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“…Since EC actively participate in local immune and inflammatory responses, differences in endothelial immunogenicity might account for vascular bed-specific variations in susceptibility to pathological conditions. Several reports over the last years, the majority derived from human umbilical vein EC (HUVEC), have demonstrated that the local flow environment influences endothelial biosecretory and immune behavior (3,5,9,12,29,31,36,39,44).Blood flow is a complex interplay of at least three distinct mechanical forces that vary in different vascular beds: hydrostatic pressure, wall shear stress, and cyclic strains (13). The EC lining acts as an integrator and transducer of these mechanical stimuli (17) and responds with flow frequency-and shear stress-dependent modulation of nitric oxide synthase activity and prostacyclin production (4, 6).…”

mentioning

confidence: 99%

mentioning

confidence: 99%

“…Yet comparable studies on regulation of endothelial adhesion molecule expression by flow greatly differ (2,5,9,12,18,19,23,29,31,36,39,44,45). The susceptibility of all EC to pathological conditions in general and the higher graft patency rates when arterial instead of venous conduits are used as bypass grafts are but isolated examples of how these findings come into clinical importance.…”

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confidence: 99%

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Vascular bed origin dictates flow pattern regulation of endothelial adhesion molecule expression

Methe¹,

Balcells²,

Alegret³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Endothelial cell phenotypes markedly differ, depending upon function and vascular bed of origin. Differences might account for specific susceptibility to pathological conditions. As leukocyte adhesion to activated endothelium is the initiating event in a range of diseases, we compared the influence of vascular bed-specific flow patterns on adhesion molecule expression in human saphenous vein (HSVEC) and coronary artery endothelial cells (HCAEC). In vitro, immune cell attachment was increased 1.6-fold when tumor necrosis factor (TNF)-␣-stimulated HSVEC were exposed to coronary artery flow in place of physiological venous flow and 1.9-fold higher compared with attachment to cytokine-stimulated HCAEC exposed to coronary artery flow. This was associated with increased concentrations of soluble E-selectin, VCAM-1, and ICAM-1 in supernatants of HSVEC exposed to coronary artery flow compared with HCAEC exposed to the same flow pattern. Venous and coronary artery flow both increased TNF-␣-induced E-selectin and ICAM-1 expression on HSVEC, but only coronary artery flow increased VCAM-1 expression. In marked contrast to HSVEC, venous and coronary artery flow attenuated TNF-␣-induced E-selectin and VCAM-1 expression on HCAEC, whereas coronary artery flow further induced ICAM-1 on cytokinestimulated HCAEC. With the exception of cytokine-induced ICAM-1, adhesion molecule expression on HSVEC exposed to coronary artery flow exceeded expression on HCAEC. Thus ICAM-1 expression involves complex flow-dependent and -independent pathways with marked dissimilarities between the two endothelial cell types studied. Interestingly, Kruppel-like factor (KLF) 4 overexpression in HCAEC and HSVEC significantly reduced TNF-␣-induced E-selectin and VCAM-1 expression in static conditions, while ICAM-1 expression remained constant. Furthermore, both flow patterns induced KLF2 and KLF4 expression in HCAEC and HSVEC. Venous and coronary artery flow differentially influence endothelial adhesion molecule and transcription factor expression, depending on the vascular bed of origin. Differences in adhesion molecule expression and subsequent immune cell adhesion between HSVEC and HCAEC may contribute to different susceptibility to pathological conditions. endothelial cells; flow shear stress ENDOTHELIAL CELLS (EC) LINE the inside of all blood vessels from the aorta to microvessels of the vasa vasorum. These cells are found in arteries and veins across a great range of sizes, local environments, and flow patterns, and as a result possess a range of phenotypes, functions, and immune and metabolic properties. While species heterogeneity has been reported (20, 35), of equal interest are differences within species where vascular bed-specific characteristics dominate (1,32,40,43). EC can attain a wide range of morphologies, create continuous or fenestrated endothelium, and express the full spectrum of regulatory proteins and subsets of antigens (32, 40). Since EC actively participate in local immune and inflammatory responses, differences in endothelial imm...

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“…In atheromas, PDGF-BB levels may not match those found to induce migration in Fig. 1g; other factors may modify migration in vivo [2,3,27].…”

Section: Pdgf-bb and Glucose Effects On Pdgf-βr Protein Levelmentioning

confidence: 89%

Glucose lowers the threshold for human aortic vascular smooth muscle cell migration: inhibition by protein phosphatase-2A

2008

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Aims/hypothesis Atherosclerosis, which occurs prematurely in individuals with diabetes, incorporates vascular smooth muscle cell (VSMC) chemotaxis. Glucose, through protein kinase C-β II signalling, increases chemotaxis to low concentrations of platelet-derived growth factor (PDGF)-BB. In VSMC, a biphasic response in PDGF-beta receptor (PDGF-βR) level occurs as PDGF-BB concentrations increase. The purpose of this study was to determine whether increased concentrations of PDGF-BB and raised glucose level had a modulatory effect on the mitogen-activated protein kinase/ extracellular-regulated protein kinase pathway, control of PDGF-βR level and chemotaxis. Methods Cultured aortic VSMC, exposed to normal glucose (NG) (5 mmol/l) or high glucose (HG) (25 mmol/l) in the presence of PDGF-BB, were assessed for migration (chemotaxis chamber) or else extracted and immunoblotted. Results At concentrations of PDGF-BB <540 pmol/l, HG caused an increase in the level of PDGF-βR in VSMC (immunoblotting) versus NG, an effect that was abrogated by inhibition of aldose reductase or protein kinase C-β II . At higher concentrations of PDGF-BB (>540 pmol/l) in HG, receptor level was reduced but in the presence of aldose reductase or protein kinase C-β II inhibitors the receptor levels increased. It is known that phosphatases may be activated at high concentrations of growth factors. At high concentrations of PDGF-BB, the protein phosphatase (PP)2A inhibitor, endothall, caused an increase in PDGF-βR levels and a loss of biphasicity in receptor levels in HG. At higher concentrations of PDGF-BB in HG, the chemoattractant effect of PDGF-BB was lost (chemotaxis chamber). Under these conditions inhibition of PP2A was associated with a restoration of chemotaxis to high concentrations of PDGF-BB. Conclusion/interpretation The biphasic response in PDGF-βR level and in chemotaxis to PDGF-BB in HG is due to PP2A activation.

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Shear stress-stimulated endothelial cells induce smooth muscle cell chemotaxis via platelet-derived growth factor-BB and interleukin-1α

Cited by 86 publications

References 63 publications

Endothelial Bmp4 Is Induced During Arterial Remodeling: Effects on Smooth Muscle Cell Migration and Proliferation

Endothelial Bmp4 Is Induced During Arterial Remodeling: Effects on Smooth Muscle Cell Migration and Proliferation

Vascular bed origin dictates flow pattern regulation of endothelial adhesion molecule expression

Glucose lowers the threshold for human aortic vascular smooth muscle cell migration: inhibition by protein phosphatase-2A

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