Coordinate Induction of the Actin Cytoskeletal Regulatory Proteins Gelsolin, Vasodilator-Stimulated Phosphoprotein, and Profilin during Capillary Morphogenesisin Vitro

Salazar, René; Bell, Scott E.; Davis, George E.

doi:10.1006/excr.1999.4460

Cited by 67 publications

(67 citation statements)

References 41 publications

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“…HUVEC suspended in gels containing rat tail collagen at 3.75-5.0 μg/ml form lumen-containing CLS within 24 hr, structures that are maintained over several days (Davis and Camarillo, 1996;Kamei et al, 2006;Salazar et al, 1999). Similar morphogenesis is observed with bovine aortic and microvascular endothelial cells plated in gels of diluted Matrigel or type I collagen (Stitt et al, 2005;A.G.…”

Section: Morphogenesismentioning

confidence: 72%

In vitro assays of angiogenesis for assessment of angiogenic and anti-angiogenic agents

Goodwin¹

2007

Microvascular Research

261

208

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Blood vessels, either in insufficient numbers or in excess, contribute to the pathogenesis of many diseases. Agents that stimulate angiogenesis can improve blood flow in patients with ischemic diseases, whereas anti-angiogenic agents are used to treat disorders ranging from macular degeneration to cancer. In this review I describe in vitro assays that can be used to assess the activity of agents that affect angiogenesis. Means of quantifying endothelial cell matrix degradation, migration, proliferation, apoptosis and morphogenesis are discussed, as are embryoid body, aortic ring and metatarsal assays of vessel outgrowth. Strengths and limitations of these techniques are also addressed.

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Section: Morphogenesismentioning

confidence: 72%

In vitro assays of angiogenesis for assessment of angiogenic and anti-angiogenic agents

Goodwin¹

2007

Microvascular Research

261

208

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“…3) (Davis and Camarillo, 1996;Salazar et al, 1999;Bayless et al, 2000;Bell et al, 2001;Rupp and Little, 2001;Bayless and Davis, 2002;Davis and Bayless, 2003). As shown in Figure 3, this pathway depends not only on EC exposure to exogenous ECM environments conducive for vascular formation such as collagen type I or fibrin matrices, but also on endogenous synthesis of ECM by ECs (Nicosia and Madri, 1987;Ingber and Folkman, 1988;Maragoudakis et al 1988;Iruela-Arispe et al, 1991;Sephel et al, 1996;Bonanno et al, 2000;Bell et al, 2001).…”

Section: Mic Signaling Axis Controls Ec Morphogenesis In Three Dimensmentioning

confidence: 99%

“…In addition, these cytoskeletal molecules control cell shape and are centrally relevant to the question of how capillary tubes form in three dimensions. Our laboratory has identified three actin regulatory proteins that are coordinately upregulated during EC morphogenesis: gelsolin, vasoactive-stimulated phosphoprotein (VASP), and profilin (Salazar et al, 1999). Gelsolin is well known to sever actin filaments, thereby participating in actin assembly/disassembly reactions; profilin binds to VASP (a major phosphoprotein target of protein kinases A and G) (Reinhard et al, 2001), and also sequesters actin monomers.…”

Section: Mic Signaling Axis Controls Ec Morphogenesis In Three Dimensmentioning

confidence: 99%

“…These matrix guidance pathways may play a key role in how ECs locate each other in 3D space and rapidly form multicellular networks in tissues. More recent assays, such as those developed by our laboratory, have utilized ECs suspended as single cells in 3D extracellular matrices (Davis and Camarillo, 1996;Salazar et al, 1999;Bayless et al, 2000;Bell et al, 2001;Bayless and Davis, 2002) (Figs. 1 and 5).…”

Section: In Vitro Models Of Capillary Morphogenesis In 3d Extracellulmentioning

confidence: 99%

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Molecular basis of endothelial cell morphogenesis in three‐dimensional extracellular matrices

2002

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Although many studies have focused on blood vessel development and new blood vessel formation associated with disease processes, the question of how endothelial cells (ECs) assemble into tubes in three dimensions (i.e., EC morphogenesis) remains unanswered. EC morphogenesis is particularly dependent on a signaling axis involving the extracellular matrix (ECM), integrins, and the cytoskeleton, which regulates EC shape changes and signals the pathways necessary for tube formation. Recent studies reveal that genes regulating this matrix-integrin-cytoskeletal (MIC) signaling axis are differentially expressed during EC morphogenesis. The Rho GTPases represent an important class of molecules involved in these events. Cdc42 and Rac1 are required for the process of EC intracellular vacuole formation and coalescence that regulates EC lumen formation in three-dimensional (3D) extracellular matrices, while RhoA appears to stabilize capillary tube networks. Once EC tube networks are established, supporting cells, such as pericytes, are recruited to further stabilize these networks, perhaps by regulating EC basement membrane matrix assembly. Furthermore, we consider recent work showing that EC morphogenesis is balanced by a tendency for newly formed tubes to regress. This morphogenesis-regression balance is controlled by differential gene expression of such molecules as VEGF, angiopoietin-2, and PAI-1, as well as a plasmin-and matrix metalloproteinase-dependent mechanism that induces tube regression through degradation of ECM scaffolds that support EC-lined tubes. It is our hope that this review will stimulate increased interest and effort focused on the basic mechanisms regulating capillary tube formation and regression in 3D extracellular matrices. Anat Rec 268: 252-275, 2002.

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“…In scars, there is a loss of normal tissue architecture and function due, at least in part, to altered cell-matrix interaction and the assembly of the actin cytoskeleton that occurs during wound repair. 1,2 The actin cytoskeleton is important in processes that are fundamental to wound healing: migration; contraction; adhesion; and proliferation. 3 The vasodilator-stimulated phosphoprotein (VASP) is associated with filamentous actin formation and likely plays a role in cell adhesion and motility.…”

mentioning

confidence: 99%

Dermal Transforming Growth Factor-β Responsiveness Mediates Wound Contraction and Epithelial Closure

Martínez‐Ferrer

Afshar-Sherif

Uwamariya

et al. 2010

The American Journal of Pathology

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Stromal-epithelial interactions are important during wound healing. Transforming growth factor-␤ (TGF-␤) signaling at the wound site has been implicated in re-epithelization , inflammatory infiltration, wound contraction , and extracellular matrix deposition and remodeling. Ultimately , TGF-␤ is central to dermal scarring. Because scarless embryonic wounds are associated with the lack of dermal TGF-␤ signaling , we studied the role of TGF-␤ signaling specifically in dermal fibroblasts through the development of a novel , inducible , conditional , and fibroblastic TGF-␤ type II receptor knockout (Tgfbr2 dermalKO ) mouse model. Full thickness excisional wounds were studied in control and Tgfbr2 dermalKO back skin. The Tgfbr2 dermalKO wounds had accelerated re-epithelization and closure compared with controls , resurfacing within 4 days of healing. The loss of TGF-␤ signaling in the dermis resulted in reduced collagen deposition and remodeling associated with a reduced extent of wound contraction and elevated macrophage infiltration. Tgfbr2 dermalKO and control skin had similar numbers of myofibroblastic cells , suggesting that myofibroblastic differentiation was not responsible for reduced wound contraction. However , several mediators of cell-matrix interaction were reduced in the Tgfbr2 dermalKO fibroblasts , including ␣1 , ␣2 , and ␤1 integrins , and collagen gel contraction was diminished. There were associated deficiencies in actin cytoskeletal organization of vasodilatorstimulated phosphoprotein-containing lamellipodia. This study indicated that paracrine and autocrine TGF-␤ dermal signaling mechanisms mediate macrophage recruitment , re-epithelization , and wound contraction. (Am J Pathol 2010, 176:98 -107;

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Coordinate Induction of the Actin Cytoskeletal Regulatory Proteins Gelsolin, Vasodilator-Stimulated Phosphoprotein, and Profilin during Capillary Morphogenesisin Vitro

Cited by 67 publications

References 41 publications

In vitro assays of angiogenesis for assessment of angiogenic and anti-angiogenic agents

In vitro assays of angiogenesis for assessment of angiogenic and anti-angiogenic agents

Molecular basis of endothelial cell morphogenesis in three‐dimensional extracellular matrices

Dermal Transforming Growth Factor-β Responsiveness Mediates Wound Contraction and Epithelial Closure

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