Vascular Endothelial Growth Factor-Induced Migration of Vascular Smooth Muscle Cells in Vitro

Grosskreutz, Cynthia L.; Anand‐Apte, Bela; Duplàa, C.; Quinn, Tim; Terman, Bruce I.; Zetter, Bruce R.; D'Amore, Patricia A.

doi:10.1006/mvre.1999.2171

Cited by 199 publications

(139 citation statements)

References 24 publications

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“…A similar observation has been reported between VEGF and ANG-2 whereby, in the presence of VEGF, ANG-2 promotes vascular sprouts whereas, in its absence, vascular regression accelerates (55,86). Hence, this window period may enable fine tuning of the neovasculature to adapt to its microenvironment through a regulated process of pruning and remodeling because these plastic vessels are likely to be more susceptible to apoptosis (87,88) The potent prosurvival effect of ANG-1 alone or in synergy with VEGF has been found to protect endothelial cells from apoptosis (91)(92)(93)(94)(95)(96). ANG-1 -mediated phosphatidylinositol 3-kinase -dependent activation of Akt and attachment to extracellular matrix are central to the survival of endothelial cells.…”

Section: Dr Jekyll and Mr Hyde In Tumor Angiogenesissupporting

confidence: 68%

Angiopoietin: A TIE(d) Balance in Tumor Angiogenesis

Shim

Wong

2007

Molecular Cancer Research

152

111

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Angiopoietins (ANG-1 and ANG-2) and their TIE-2 receptor tyrosine kinase have wide-ranging effects on tumor malignancy that includes angiogenesis, inflammation, and vascular extravasation. These multifaceted pathways present a valuable opportunity in developing novel inhibition strategies for cancer treatment. However, the regulatory role of ANG-1 and ANG-2 in tumor angiogenesis remains controversial. There is a complex interplay between complementary yet conflicting roles of both the ANGs in shaping the outcome of angiogenesis. Embryonic vascular development suggests that ANG-1 is crucial in engaging interaction between endothelial and perivascular cells. However, recruitment of perivascular cells by ANG-1 has recently been implicated in its antiangiogenic effect on tumor growth. It is becoming clear that TIE-2 signaling may function in a paracrine and autocrine manner directly on tumor cells because the receptor has been increasingly found in tumor cells. In addition, A 5 B 1 and A v B 5 integrins were recently recognized as functional receptors for ANG-1 and ANG-2. Therefore, both the ligands may have wide-ranging functions in cellular activities that affect overall tumor development. Collectively, these TIE-2 -dependent and TIE-2 -independent activities may account for the conflicting findings of ANG-1 and ANG-2 in tumor angiogenesis. These uncertainties have impeded development of a clear strategy to target this important angiogenic pathway. A better understanding of the molecular basis of ANG-1 and ANG-2 activity in the pathophysiologic regulation of angiogenesis may set the stage for novel therapy targeting this pathway. (Mol Cancer Res 2007;5(7):655 -65)

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Section: Dr Jekyll and Mr Hyde In Tumor Angiogenesissupporting

confidence: 68%

Angiopoietin: A TIE(d) Balance in Tumor Angiogenesis

Shim

Wong

2007

Molecular Cancer Research

152

111

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“…The prolonged duration of hVEGF 165 Targeted VEGF delivery to myocardium G Korpanty et al expression with UTMD may also facilitate the previously described protective effect of smooth muscle cellendothelial cell interactions on the newly formed microcirculation and its important role in the vascular remodeling. [19][20][21][22] We did not observe any increase in capillary or arteriolar density with either hVEGF 165 plasmid alone, or with microbubble destruction alone. It is not surprising that i.v.…”

Section: Discussionmentioning

confidence: 88%

Targeting of VEGF-mediated angiogenesis to rat myocardium using ultrasonic destruction of microbubbles

et al. 2005

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Myocardial angiogenesis mediated by human vascular endothelial growth factor 165 (hVEGF 165 ) cDNA was promoted in rat myocardium using an in vivo-targeted gene delivery system known as ultrasound-targeted microbubble destruction (UTMD). Microbubbles carrying plasmids encoding hVEGF 165 , or control solutions were infused intravenously during ultrasonic destruction of the microbubbles within the myocardium. Biochemical and histological assessment of gene expression and angiogenesis were performed 5, 10, and 30 days after UTMD. UTMD-treated myocardium contained hVEGF 165 protein and mRNA. The myocardium of UTMD-treated animals showed hypercellular foci associated with hVEGF 165 expression and endothelial cell markers. Capillary density in UTMD-treated rats increased 18% at 5 days and 33% at 10 days, returning to control levels at 30 days (Po0.0001). Similarly, arteriolar density increased 22% at 5 days, 86% at 10 days, and 31% at 30 days (Po0.0001). Thus, noninvasive delivery of hVEGF 165 to rat myocardium by UTMD resulted in significant increases in myocardial capillary and arteriolar density.

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“…Although VEGF does not induce SMC proliferation, VEGF could increase SMC migration directly or indirectly by triggering the release of platelet-derived growth factor-BB from adjacent cells. 6,7,25 VEGF may also enhance VEGFR receptor-1-mediated infiltration of macrophages and VEGFR-2-mediated migration of endothelial and smooth muscle progenitor cells from bone marrow into the graft, which may contribute to the formation of transplant coronary arteriosclerosis. 5,26 -28 VEGF is also a proinflammatory cytokine and stimulates expression of intracellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin on endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…4,5 VEGF does not induce proliferation of smooth muscle cells (SMCs) but is a chemoattractant to them and facilitates their migration by matrix metalloproteinase production. 6,7 Preclinical and clinical therapeutic approaches show that VEGF promotes neovascularization in ischemic myocardial and peripheral vascular limb disease and that it improves endothelium-dependent vasorelaxation. 8 -13 Furthermore, studies with both recombinant protein and arterial gene transfer demonstrate that VEGF enhances reendothelialization and thereby reduces intimal thickening in arterial restenosis and after stent implantation.…”

mentioning

confidence: 99%

Vascular Endothelial Growth Factor Enhances Cardiac Allograft Arteriosclerosis

et al. 2002

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Background-Cardiac allograft arteriosclerosis is a complex process of alloimmune response, chronic inflammation, and smooth muscle cell proliferation that includes cross talk between cytokines and growth factors. Methods and Results-Our results in rat cardiac allografts established alloimmune response as an alternative stimulus capable of inducing vascular endothelial growth factor (VEGF) mRNA and protein expression in cardiomyocytes and graft-infiltrating mononuclear inflammatory cells, which suggests that these cells may function as a source of VEGF to the cells of coronary arteries. Linear regression analysis of these allografts with different stages of arteriosclerotic lesions revealed a strong correlation between intragraft VEGF protein expression and the development of intimal thickening, whereas blockade of signaling downstream of VEGF receptor significantly reduced arteriosclerotic lesions. In addition, in cholesterol-fed rabbits, intracoronary perfusion of cardiac allografts with a clinical-grade adenoviral vector that encoded mouse VEGF 164 enhanced the formation of arteriosclerotic lesions, possibly secondary to increased intragraft influx of macrophages and neovascularization in the intimal lesions. Conclusions-Our findings suggest a positive regulatory role between VEGF and coronary arteriosclerotic lesion formation in the allograft cytokine microenvironment.

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Vascular Endothelial Growth Factor-Induced Migration of Vascular Smooth Muscle Cells in Vitro

Cited by 199 publications

References 24 publications

Angiopoietin: A TIE(d) Balance in Tumor Angiogenesis

Angiopoietin: A TIE(d) Balance in Tumor Angiogenesis

Targeting of VEGF-mediated angiogenesis to rat myocardium using ultrasonic destruction of microbubbles

Vascular Endothelial Growth Factor Enhances Cardiac Allograft Arteriosclerosis

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