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367
Regulation of wound healing by growth factors and cytokines
- Physiol. Rev
, 2003
"... II. Platelet-Derived Growth Factor Family 838 A. Expression of PDGF at the wound site 838 B. Inhibition of PDGF action in healing skin wounds 839 III. Fibroblast Growth Factor Family 839 ..."
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II. Platelet-Derived Growth Factor Family 838 A. Expression of PDGF at the wound site 838 B. Inhibition of PDGF action in healing skin wounds 839 III. Fibroblast Growth Factor Family 839
Chemokines in cutaneous wound healing
- J. Leukoc. Biol
, 2001
"... Abstract: Healing of wounds is one of the most complex biological events after birth as a result of the interplay of different tissue structures and a large number of resident and infiltrating cell types. The latter are mainly constituted by leukocyte subsets (neutrophils, macrophages, mast cells, a ..."
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Cited by 84 (0 self)
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Abstract: Healing of wounds is one of the most complex biological events after birth as a result of the interplay of different tissue structures and a large number of resident and infiltrating cell types. The latter are mainly constituted by leukocyte subsets (neutrophils, macrophages, mast cells, and lymphocytes), which sequentially infiltrate the wound site and serve as immunological effector cells but also as sources of inflammatory and growth-promoting cytokines. Recent data demonstrate that recruitment of leukocyte subtypes is tightly regulated by chemokines. Moreover, the presence of chemokine receptors on resident cells (e.g., keratinocytes, endothelial cells) indicates that chemokines also contribute to the regulation of epithelialization, tissue remodeling, and angiogenesis. Thus, chemokines are in an exclusive position to integrate inflammatory events and reparative processes and are important modulators of human-skin wound healing. This review will focus preferentially on the role of chemokines during skin wound healing and intends to provide an update on the multiple functions of individual chemokines during the phases of wound repair. J. Leukoc.
Up- regulation of vascular endothelial growth factor and its cognate receptors in a rat glioma model of tumor angiogenesis
- Cancer Res
, 1993
"... Capillary hemangioblastoma is the most frequent manifestation of the autosomal dominantly inherited von Hippel-Lindau (VHL) disease but also presents as a nonfamilial, sporadic vascular tumor. Hemangioblasto mas are characterized by a dense network of capillaries in association with cysts. To invest ..."
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Cited by 58 (2 self)
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Capillary hemangioblastoma is the most frequent manifestation of the autosomal dominantly inherited von Hippel-Lindau (VHL) disease but also presents as a nonfamilial, sporadic vascular tumor. Hemangioblasto mas are characterized by a dense network of capillaries in association with cysts. To investigate the mechanisms underlying neovascularization and cyst formation, we analyzed eight VHL disease-associated and five spo radic hemangioblastomas. Histologically, both tumor types showed a sim ilar phenotype. The capillaries expressed the endothelial cell markers von Willebrand factor and CD31 antigen. We investigated the expression of vascular endothelial growth factor (VEGF), an endothelial cell-specific mitogen which is also known to induce vascular permeability in vivo, and its high affinity tyrosine kinase receptors.//'- / and r\l>K. Northern blot and
Vascular endothelial growth factor induces VE-cadherin tyrosine phosphorylation in endothelial cells
- J. Cell Sci
, 1998
"... Abstract. Vascular endothelial growth factor (VEGF) is an important regulator of vasculogenesis, angiogenesis, and vascular permeability. In contrast to its transient expression during the formation of new blood vessels, VEGF and its receptors are continuously and highly expressed in some adult tiss ..."
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Cited by 57 (1 self)
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Abstract. Vascular endothelial growth factor (VEGF) is an important regulator of vasculogenesis, angiogenesis, and vascular permeability. In contrast to its transient expression during the formation of new blood vessels, VEGF and its receptors are continuously and highly expressed in some adult tissues, such as the kidney glomerulus and choroid plexus. This suggests that VEGF produced by the epithelial cells of these tissues might be involved in the induction or maintenance of fenestrations in adjacent endothelial cells expressing the VEGF receptors. Here we describe a defined in vitro culture system where fenestrae formation was induced in adrenal cortex capillary endothelial cells by VEGF, but not by fibroblast growth factor. A strong induction of endothelial fenestrations was observed in
Angiogenesis: potentials for pharmacologic intervention in the treatment of cancer, cardiovascular diseases, and chronic inflammation, Pharmacol
- Rev
"... Abstract................................................................................ 238 I. General aspects of angiogenesis........................................................... 238 A. Introduction......................................................................... 238 B. Function of e ..."
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Cited by 48 (6 self)
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Abstract................................................................................ 238 I. General aspects of angiogenesis........................................................... 238 A. Introduction......................................................................... 238 B. Function of endothelial cells in normal physiology....................................... 239 C. Molecular control of angiogenesis...................................................... 239 1. Initiation of the angiogenic response................................................ 239 2. Endothelial cell migration and proliferation.......................................... 240
Epidemiology and prevention of ovarian hyperstimulation syndrome (OHSS): a review. Hum Reprod Update 2002;8:559–77
"... Ovarian hyperstimulation syndrome (OHSS) is a rare iatrogenic complication of ovarian stimulation occurring during the luteal phase or during early pregnancy. Fortunately, the reported prevalence of the severe form of OHSS is small, ranging from 0.5 to 5%. Nevertheless, as this is an iatrogenic comp ..."
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Cited by 43 (1 self)
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Ovarian hyperstimulation syndrome (OHSS) is a rare iatrogenic complication of ovarian stimulation occurring during the luteal phase or during early pregnancy. Fortunately, the reported prevalence of the severe form of OHSS is small, ranging from 0.5 to 5%. Nevertheless, as this is an iatrogenic complication of a non-vital treatment with a potentially fatal outcome, the syndrome remains a serious problem for specialists dealing with infertility. The aim of this literature review was to determine whether it is possible to identify patients at risk, and which preventive method should be applied when an exaggerated ovarian response occurs. Data pertaining to the epidemiology and prevention of OHSS in women were searched using Medline, Current Contents and PubMed, and are summarized. Preventive strategies attempt either to limit the dose or concentration of hCG or to ®nd a way to induce luteolysis without inducing a detrimental effect on endometrial and oocyte quality. The following particular preventive strategies were reviewed: cancelling the cycle; coasting; early unilateral ovarian follicular aspiration (EUFA); modifying the methods of ovulation triggering; administration of glucocorticoids, macromolecules and progesterone;
Lack of pericytes leads to endothelial hyperplasia and abnormal vascular morphogenesis
- J. Cell
, 2001
"... Abstract. The association of pericytes (PCs) to newly formed blood vessels has been suggested to regulate endothelial cell (EC) proliferation, survival, migration, differentiation, and vascular branching. Here, we addressed these issues using PDGF-B – and PDGF receptor-� (PDGFR-�)–deficient mice as ..."
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Cited by 42 (1 self)
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Abstract. The association of pericytes (PCs) to newly formed blood vessels has been suggested to regulate endothelial cell (EC) proliferation, survival, migration, differentiation, and vascular branching. Here, we addressed these issues using PDGF-B – and PDGF receptor-� (PDGFR-�)–deficient mice as in vivo models of brain angiogenesis in the absence of PCs. Quantitative morphological analysis showed that these mutants have normal microvessel density, length, and number of branch points. However, absence of PCs correlates with endothelial hyperplasia, increased capillary diameter, abnormal EC shape and ultrastructure, changed cellular distribution of certain junctional proteins, and morphological signs of increased transendothelial permeability. Brain endothelial hyperplasia was observed already at embryonic day (E) 11.5 and persisted throughout development. From E 13.5, vascular endothelial growth factor-A (VEGF-A) and other genes responsive to metabolic stress became upregulated, suggesting that the abnormal microvessel architecture has systemic metabolic consequences. VEGF-A upregulation correlated temporally with the occurrence of vascular abnormalities in the placenta and dilation of the heart. Thus, although PC deficiency appears to have direct effects on EC number before E 13.5, the subsequent increased VEGF-A levels may further abrogate microvessel architecture, promote vascular permeability, and contribute to formation of the edematous phenotype observed in late gestation PDGF-B and PDGFR- � knock out embryos. Key words: mice • angiogenesis • pericytes • plateletderived growth factor B • vascular endothelial growth factor
A role for tissue factor in cell adhesion and migration mediated by interaction with actin-binding protein 280
- J Cell Biol
, 1998
"... Tissue factor (TF), the protease receptor ini-tiating the coagulation system, functions in vascular de-velopment, angiogenesis, and tumor cell metastasis by poorly defined molecular mechanisms. We demon-strate that immobilized ligands for TF specifically sup-port cell adhesion, migration, spreading, ..."
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Cited by 40 (5 self)
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Tissue factor (TF), the protease receptor ini-tiating the coagulation system, functions in vascular de-velopment, angiogenesis, and tumor cell metastasis by poorly defined molecular mechanisms. We demon-strate that immobilized ligands for TF specifically sup-port cell adhesion, migration, spreading, and intracellu-lar signaling, which are not inhibited by RGD peptides. Two-hybrid screening identified actin-binding protein 280 (ABP-280) as ligand for the TF cytoplasmic do-main. Extracellular ligation of TF is necessary for ABP-280 binding. ABP-280 recruitment to TF adhesion con-tacts is associated with reorganization of actin fila-ments, but cytoskeletal adaptor molecules typically found in integrin-mediated focal contacts are not asso-ciated with TF. Chimeric molecules of the TF cytoplas-mic domain and an unrelated extracellular domain sup-port cell spreading and migration, demonstrating that the extracellular domain of TF is not involved in the re-cruitment of accessory molecules that influence adhe-sive functions. Replacement of TF’s cytoplasmic Ser residues with Asp to mimic phosphorylation enhances the interaction with ABP-280, whereas Ala mutations abolish coprecipitation of ABP-280 with immobilized TF cytoplasmic domain, and severely reduce cell spreading. The specific interaction of the TF cytoplas-mic domain with ABP-280 provides a molecular path-way by which TF supports tumor cell metastasis and vascular remodeling.
Humanization of an anti-vascular endothelial growth factor monoclonal antibody for the therapy of solid tumors and other disorders
- Cancer Res
, 1997
"... Vascular endothelial growth factor (VE(ìF)is a major mediator of angiogenesis associated with tumors and other pathological conditions, including proliferative diahetic retinopathy and age-related macular degeneration. The murine anti-human \ I (.1 monoclonal antibody imiiM \l> \ I.di i A.4.6.1 ..."
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Cited by 39 (1 self)
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Vascular endothelial growth factor (VE(ìF)is a major mediator of angiogenesis associated with tumors and other pathological conditions, including proliferative diahetic retinopathy and age-related macular degeneration. The murine anti-human \ I (.1 monoclonal antibody imiiM \l> \ I.di i A.4.6.1 has heen shown to potently suppress angiogenesis and growth in a variety of human tumor cells lines transplanted in nude mice and also to inhibit neovascularization in a primate model of ischemie retinal disease. In this report, we describe the humanization of muMAb VEGF A.4.6.1. by site-directed mutagenesis of a human framework. Not only the residues involved in the six complementaritydetermining regions but also several framework residues were changed from human to murine. Humanized anti-V'EGF F(ab) and Ig(ìlvari ants bind \ 1 (.1 with affinity very similar to that of the original murine antibody. Furthermore, recomhinant humanized MAb VEGF
