Angiogenesis in vitro

Folkman, Judah; Haudenschild, Christian C.

doi:10.1038/288551a0

Cited by 983 publications

(522 citation statements)

References 14 publications

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“…In the present study, we have demonstrated for the first time that AGE, nonenzymatically glycated protein derivatives formed under hyperglycemia, stimulate the growth and tube formation of human microvascular endothelial cells, the key steps of angiogenesis which take place in this very cell type (33,34). The present findings have extended our preliminary work employing endothelial cells from a larger vessel, i.e.…”

Section: Discussionsupporting

confidence: 74%

Advanced Glycation End Products-driven Angiogenesis in Vitro

Yamagishi

Yonekura

Yamamoto

et al. 1997

Journal of Biological Chemistry

260

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This study was undertaken to determine whether and how advanced glycation end products (AGE), senescent macroproteins accumulated in various tissues under hyperglycemic states, cause angiogenesis, the principal vascular derangement in diabetic microangiopathy. We first prepared AGE-bovine serum albumin (BSA) and anti-AGE antiserum using AGE-RNase A. Then AGE-BSA was administered to human skin microvascular endothelial cells in culture, and their growth was examined. The AGE-BSA, but not nonglycated BSA, was found to induce a statistically significant increase in the number of viable endothelial cells as well as their synthesis of DNA. The increase in DNA synthesis by AGE-BSA was abolished by anti-AGE antibodies. AGE-BSA also stimulated the tube formation of endothelial cells on Matrigel. We obtained the following evidence that it is vascular endothelial growth factor (VEGF) that mainly mediates the angiogenic activities of AGE. Glucose and other reducing sugars can react nonenzymatically with the amino groups of proteins to form reversible Schiff bases and, then, Amadori products. These early glycation products undergo further complex reactions such as rearrangement, dehydration, and condensation to become irreversibly crosslinked, heterogeneous fluorescent derivatives termed advanced glycation end products (AGE) 1 (1). The formation and accumulation of AGE in various tissues have been known to progress during normal aging and at an extremely accelerated rate in diabetes mellitus. This has been implicated in the development of diabetic micro-and macro-vascular complications (1), which may account for the disabilities and high mortality rate in patients with this disease (2).Microvessels are composed of only two types of cells, endothelial cells and pericytes, and have been known to show both functional and structural abnormalities during prolonged diabetic exposure, resulting in the deleterious effects on the organs that they supply (3-5). Using pericyte-endothelial cell co-culture systems, we have shown previously that pericytes can not only regulate the growth but also preserve the prostacyclin-producing ability and protect against lipid peroxide-induced injury of endothelial cells (6). This has provided a basis for understanding how diabetic retinopathy develops consequent to "pericyte loss," the earliest histopathological hallmark in diabetic retinopathy (5, 7).Recently, we have found that AGE exert a growth inhibitory effect and a cell type-specific immediate toxicity on pericytes through interactions with their receptor for AGE (RAGE), a cell surface receptor belonging to the immunoglobulin superfamily (8), and have proposed a novel mechanism for pericyte loss (9). The AGE-induced, RAGE-mediated decrease in pericyte number would then indirectly cause angiogenesis (6,9).In the present study, we investigated the effects of AGE on the growth and tube formation of human skin microvascular endothelial cells, the key steps of angiogenesis. We demonstrate that AGE exert angiogenic activities directly on microvasc...

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Section: Discussionsupporting

confidence: 74%

Advanced Glycation End Products-driven Angiogenesis in Vitro

Yamagishi

Yonekura

Yamamoto

et al. 1997

Journal of Biological Chemistry

260

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“…As is widely known, angiogenesis depends on endothelial cell survival, migration and formation of new blood vessels (Folkman and Haudenschild, 1980). For this reason, endothelial tube formation assay is frequently adopted to demonstrate angiogenesis in vitro (Kubota et al, 1988).…”

Section: Pi4kiia Is Correlated With and Has A Crucial Role In Tumor Gmentioning

confidence: 99%

PI4KIIα is a novel regulator of tumor growth by its action on angiogenesis and HIF-1α regulation

Zhang

et al. 2010

Oncogene

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“…Also, these networks in young cultures encircled subpopulations of tumor cells and varied widely in lumen diameter. By comparison, endothelial cell cords in vitro typically demonstrate a more uniform diameter on most matrices [37][38][39][40] and most, if not all, of the cultured endothelial cells typically participate in cord formation under identical media and matrix conditions without encircling subpopulations of endothelial cells ( Figure 5C). The presence of spheroidal cell nests within the boundaries formed by tumor cell cords is not a characteristic feature of endothelial cord formation in Matrigel or on other matrices (compare Figure 5A with Figure 5C).…”

Section: Biomechanical Potential Of Highly Invasive and Poorly Invasimentioning

confidence: 99%

Vascular Channel Formation by Human Melanoma Cells in Vivo and in Vitro: Vasculogenic Mimicry

Maniotis

Folberg

Hess

et al. 1999

The American Journal of Pathology

1,685

1,572

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Tissue sections from aggressive human intraocular (uveal) and metastatic cutaneous melanomas generally lack evidence of significant necrosis and contain patterned networks of interconnected loops of extracellular matrix. The matrix that forms these loops or networks may be solid or hollow. Red blood cells have been detected within the hollow channel components of this patterned matrix histologically, and these vascular channel networks have been detected in human tumors angiographically. Endothelial cells were not identified within these matrix-embedded channels by light microscopy , by transmission electron microscopy , or by using an immunohistochemical panel of endothelial cell markers (Factor VIIIrelated antigen , Ulex , CD31 , CD34 , and KDR[Flk-1]). Highly invasive primary and metastatic human melanoma cells formed patterned solid and hollow matrix channels (seen in tissue sections of aggressive primary and metastatic human melanomas) in threedimensional cultures containing Matrigel or dilute Type I collagen , without endothelial cells or fibroblasts. These tumor cell-generated patterned channels conducted dye , highlighting looping patterns visualized angiographically in human tumors. Neither normal melanocytes nor poorly invasive melanoma cells generated these patterned channels in vitro under identical culture conditions , even after the addition of conditioned medium from metastatic pattern- It is generally assumed that tumors require a blood supply for growth and metastasis. 1 The development of the tumor microcirculation compartment includes both the production of new blood vessels (angiogenesis) and their remodeling. 2 In fact, the number of vessels 3 and the patterning of the microcirculation 4 by remodeling events are used as histological markers of tumor progression. Although attention has been focused on factors that stimulate and suppress tumor angiogenesis, the molecular mechanisms underlying tumor remodeling remain enigmatic. It is therefore critical to investigate remodeling of the intratumoral microvasculature in various tumor models.Melanoma is among the better characterized tumor models with respect to prognostic staging of disease progression. The rising incidence of cutaneous melanoma makes this tumor an important public health problem. Melanoma of the interior of the eye, uveal melanoma, although much less common than cutaneous melanoma, poses a threat to vision and significant morbidity; nearly 50% of patients with uveal melanoma die from metastatic melanoma. 5 Cutaneous melanoma may disseminate through lymphatics or blood vessels. In contrast, the interior of the eye lacks lymphatics, and uveal melanoma, which develops in one of the most capillary-rich tissues of the body, is a paradigm for pure hematogeneous dissemination of cancer. 6 Therefore, the development of a tumor microcirculation in uveal melanoma is a rate-limiting step for hematological metastasis and serves as an important model for study of the cellular and molecular infrastruc-

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Angiogenesis in vitro

Cited by 983 publications

References 14 publications

Advanced Glycation End Products-driven Angiogenesis in Vitro

Advanced Glycation End Products-driven Angiogenesis in Vitro

PI4KIIα is a novel regulator of tumor growth by its action on angiogenesis and HIF-1α regulation

Vascular Channel Formation by Human Melanoma Cells in Vivo and in Vitro: Vasculogenic Mimicry

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