Linked Life Data

17136757

Source:http://linkedlifedata.com/resource/pubmed/id/17136757

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-12-5
pubmed:abstractText
Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis during the wound healing process. As epithelial-mesenchymal interactions have been shown to regulate a plethora of genes in wound healing, we hypothesized that these interactions might have a role in modulating VEGF expression and angiogenesis. A two chamber co-culture model was used, wherein normal and keloid keratinocytes and fibroblasts were physically separated by membrane inserts while allowing cytokine diffusion. Cell lysates obtained from keratinocytes co-cultured with fibroblasts demonstrated increased expression of VEGF. An enzyme-linked immunosorbent assay (ELISA) showed significant increase in VEGF expression in co-culture conditioned media compared with controls. Additionally, the conditioned medium from keloid keratinocyte and fibroblast co-cultures increased proliferation and formation of complex three-dimensional capillary-like structures in human umbilical vein endothelial cells, emphasising the importance of epithelial-mesenchymal interactions in the angiogenic process. Immunostaining of keloid tissue localized VEGF in the basal layer of the epidermis and also demonstrated higher blood vessel density than normal skin. Keloid tissue extract also demonstrated increased expression of VEGF compared with normal skin. It is likely that epidermal VEGF exerts significant paracrine control over the dynamics and expression profile of underlying dermal fibroblasts. Addition of the inhibitors WP631, mitoxantrone, and Rapamycin to keloid keratinocyte and fibroblast co-cultures, downregulated secreted VEGF expression in a dose-dependent manner, suggesting therapeutic potential for these compounds in the treatment of keloid scars.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-3417
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2006 Pathological Society of Great Britain and Ireland.
pubmed:issnType
Print
pubmed:volume
211
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
95-108
pubmed:meshHeading
pubmed-meshheading:17136757-Antibiotics, Antineoplastic, pubmed-meshheading:17136757-Antineoplastic Agents, pubmed-meshheading:17136757-Cell Differentiation, pubmed-meshheading:17136757-Cell Proliferation, pubmed-meshheading:17136757-Coculture Techniques, pubmed-meshheading:17136757-Culture Media, Conditioned, pubmed-meshheading:17136757-Daunorubicin, pubmed-meshheading:17136757-Dose-Response Relationship, Drug, pubmed-meshheading:17136757-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:17136757-Epithelial Cells, pubmed-meshheading:17136757-Fibroblasts, pubmed-meshheading:17136757-Humans, pubmed-meshheading:17136757-Immunohistochemistry, pubmed-meshheading:17136757-Keloid, pubmed-meshheading:17136757-Keratinocytes, pubmed-meshheading:17136757-Mesoderm, pubmed-meshheading:17136757-Mitoxantrone, pubmed-meshheading:17136757-Neovascularization, Pathologic, pubmed-meshheading:17136757-Sirolimus, pubmed-meshheading:17136757-Statistics, Nonparametric, pubmed-meshheading:17136757-Up-Regulation, pubmed-meshheading:17136757-Vascular Endothelial Growth Factor A, pubmed-meshheading:17136757-Wound Healing
pubmed:year
2007
pubmed:articleTitle
Epithelial-mesenchymal interactions in keloid pathogenesis modulate vascular endothelial growth factor expression and secretion.
pubmed:affiliation
Department of Surgery, National University of Singapore, Singapore.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't