Organized type I collagen influences endothelial patterns during “spontaneous angiogenesis in vitro”: Planar cultures as models of vascular development

Vernon, Robert B.; Lara, Stephanie; Drake, Christopher J.; Iruela‐Arispe, M. Luisa; Angello, John C.; Little, Charles D.; Wight, Thomas N.; Sage, E. Helene

doi:10.1007/bf02633972

Cited by 139 publications

(94 citation statements)

References 39 publications

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“…A daily administration of ACTH-(1-39) during 7 days fully restored plasma corticosterone level to control levels and partially restored adrenal weight from 5.4 Ϯ 0.62 mg (n ϭ 10) (DEX) to 7.5 Ϯ 0.5 mg (n ϭ 10), whereas the expression of the ACTH receptor was ϳ65% of the control value (P Ͻ 0.05). These results are consistent with in vitro observations demonstrating that ACTH receptor mRNA levels were stimulated by ACTH in cultures of human and bovine adrenocortical cells (32,48). All together, these data show that the glucocorticoid treatment of mice inhibits adrenal growth and steroid production, which gives an interesting model of hormonal regulation of the adrenal, because ACTH administration completely restored corticosterone production and stimulated adrenal growth.…”

Section: Vegf and Its Two High-affinity Receptors Flk-1/kdr And Flt-supporting

confidence: 91%

“…The growth of new vascular sprouts from existent vasculature is referred to as angiogenesis. The morphogenetic and regulatory processes that mediate and control an- (48). To determine whether steroidogenic cells could regulate endothelial cells in the adrenal cortex, we examined whether ACE cells exhibited changes in cellular morphology and orientation, which characterizes angiogenesis in vitro when cocultured with steroidogenic cells in 3D-collagen.…”

Section: Vegf and Its Two High-affinity Receptors Flk-1/kdr And Flt-mentioning

confidence: 99%

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Differential expression of VEGF receptors in adrenal atrophy induced by dexamethasone: a protective role of ACTH

Mallet

Féraud²,

Ouengue-Mbélé

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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Mallet, Christine, Olivier Fé raud, Gaehl OuengueMbé lé , Isabelle Gaillard, Nicolas Sappay, Daniel Vittet, and Isabelle Vilgrain. Differential expression of VEGF receptors in adrenal atrophy induced by dexamethasone: a protective role of ACTH. Am J Physiol Endocrinol Metab 284: E156-E167, 2003; 10.1152/ajpendo.00450.2001.-Although ACTH is important to adrenal growth and steroidogenesis, its role in vascular development and function has not been established in vivo. In the present study, we demonstrate the expression of mRNA for all four VEGF isoforms (mVEGF120, 144, 164, 188) and for Flk-1/KDR and Flt-1 receptors in the mouse adrenal in vivo. Suppression of the pituitary adrenocortical axis by dexamethasone (0.5 mg ⅐ 100 g body wt Ϫ1 ⅐ day Ϫ1 during 6 days) induced a decrease in corticosterone levels, adrenal weights by 50% (P Ͻ 0.001), VEGF188 mRNA, and Flk-1/KDR mRNA, whereas Flt-1 remained consistent during steroid treatment. A daily injection of ACTH-(1-39) restored the transcript for Flk-1/KDR and both VEGF188 and plasma corticosterone to control levels. To gain further insights into the effects of ACTH, cultured endothelial cells (ECs) were treated with forskolin, which increases cAMP, the second messenger in ACTH action. We demonstrate that Flk-1/KDR protein expression was markedly increased by forskolin within 24-48 h of treatment in a dose-dependent manner (0.1-10 M). The biological effect of ACTH on ECs was then tested by use of coincubations of fasciculata cells and ECs in 3D-collagen assay. Within 5-7 days of culture, ECs organized into multicellular structures that resemble networks of microvasculature, which characterize angiogenesis in vitro. vascular endothelial growth factor receptors; adrenocorticotropin; angiogenesis; mouse adrenal; steroidogenesis; hypothalamo-pituitary disconnection; vascular permeability THE ADRENAL CORTEX is physiologically important as the site of formation and secretion of several steroid hormones and less-active steroids. The secreted hormones gain access to the bloodstream through an intense and complex adrenal vasculature that is essential for organ growth and maintenance. The vessels of the adrenal cortex are characterized by richly fenestrated endothelia (2, 40). These fenestrations are the pores through which releasing factors within the hemal milieu can access the cells. In adult mammals, adrenal growth and steroidogenesis are regulated by adrenocorticotropin (ACTH) (27), which acts through interaction with a specific melanocortin receptor (MC2R) specifically expressed in the adrenal cortex (6, 32). This guanine nucleotide-binding protein-coupled receptor elicits the activation of adenylate cyclase and the production of cAMP, which activate the protein kinase A-signaling pathway (39, 53) and the normal functioning of adrenocortical cells. Glucocorticoid hormones are thought to exert negative feedback inhibition on hypothalamic-pituitary-adrenocortical axis activity at the pituitary, hypothalamic, and extrahypothalamic levels. This ultimately results in decreased...

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Section: Vegf and Its Two High-affinity Receptors Flk-1/kdr And Flt-supporting

confidence: 91%

Section: Vegf and Its Two High-affinity Receptors Flk-1/kdr And Flt-mentioning

confidence: 99%

Differential expression of VEGF receptors in adrenal atrophy induced by dexamethasone: a protective role of ACTH

Mallet

Féraud²,

Ouengue-Mbélé

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

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“…During angiogenesis, proliferating ECs are organized to form new 3-dimensional capillary networks through a process involving transition of endothelial precursor cells to spindleshape morphology in combination with alignment into solid, multicellular, precapillary, cordlike structures. Moreover, these cordlike structures are interconnected to form a polygonal network (18,19). Previous studies revealed that GTPase RhoA mediates cell contractility by organizing actin filaments into stress fibers; and active RhoA is required for a variety of complex morphogenetic processes, including embryonic gastrulation and epidermal wound healing (20,21).…”

Section: Discussionmentioning

confidence: 99%

“…The 3-dimensional type I collagen provokes ECs in culture to undergo marked shape changes that closely imitate precapillary cord formation in vivo (18). Therefore, we designed a strategy to investigate vascular morphogenesis by embedding ECs in collagen I to investigate the effects of RhoA on EC organizational behavior.…”

Section: Rhoa Expression On the Pegfp-c1-mentioning

confidence: 99%

The effect of RhoA on human umbilical vein endothelial cell migration and angiogenesis in vitro

Zhao

Xu²,

Zhou³

et al. 2006

Oncol Rep

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Abstract. The mechanisms that control the morphologic organization of endothelial cells (ECs) into new blood vessels are not well understood. Recent studies revealed that the small G proteins of the Rho family are key regulators of cell migration, involving reorganization of the actin cytoskeleton, cell migration and the regulation of gene transcription. We hypothesized that RhoA GTPase, a member of the Rho family, may play an important role in EC organization during angiogenesis, the process of new vessel formation in preexisting tissues. To test this hypothesis, we investigated the effects of RhoA on human umbilical vein endothelial (HUVE) cell migration and angiogenesis in vitro, by stably transfecting HUVE cells with sense RhoA expression plasmid through the Lipofect-2000 system. Wound assay in vitro and 3-dimensional cell culture were used to detect the migration and angiogenesis capacity of HUVE cells. The morphological changes of transfected cells were revealed under confocal and phase contrast microscopy. Our results demonstrated that the increased expression of RhoA in HUVE cells significantly enhanced the morphogenetic changes and cytoskeletal reorganization of the transfected cells, and also enhanced cell migration and angiogenic capacity in vitro, suggesting that RhoA plays an important role in the process of HUVE cell migration and angiogenesis in vitro.

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“…38,41 In addition, highly invasive melanoma cells have been demonstrated to contract floating collagen gels. 42 Because we observed that highly invasive melanoma cells could generate patterned vessels in vitro, we explored the ability of these cells to contract floating matrices as evidence of their matrix remodeling potential.…”

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

1,735

1,636

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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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Organized type I collagen influences endothelial patterns during “spontaneous angiogenesis in vitro”: Planar cultures as models of vascular development

Cited by 139 publications

References 39 publications

Differential expression of VEGF receptors in adrenal atrophy induced by dexamethasone: a protective role of ACTH

Differential expression of VEGF receptors in adrenal atrophy induced by dexamethasone: a protective role of ACTH

The effect of RhoA on human umbilical vein endothelial cell migration and angiogenesis in vitro

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

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