Linked Life Data

16002726

Source:http://linkedlifedata.com/resource/pubmed/id/16002726

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-7-8
pubmed:abstractText
Vascular endothelial growth factor (VEGF) is an angiogenesis factor with proinflammatory roles. Flt-1 is one of the specific receptors for VEGF, and soluble flt-1 (sflt-1) binds to VEGF and competitively inhibits it from binding to the receptors. We examined the role of VEGF in the pathophysiology of bleomycin-induced pneumopathy in mice, using a new therapeutic strategy that comprises transfection of the sflt-1 gene into skeletal muscles as a biofactory for anti-VEGF therapy. The serum levels of sflt-1 were significantly increased at 3-14 days after the gene transfer. Transfection of the sflt-1 gene at 3 days before or 7 days after the intratracheal instillation of bleomycin decreased the number of inflammatory cells, the protein concentration in the bronchoalveolar lavage fluid and with von Willebrand factor expression at 14 days. Transfection of the sflt-1 gene also attenuated pulmonary fibrosis and apoptosis at 14 days. Since the inflammatory cell infiltration begins at 3 days and is followed by interstitial fibrosis, it is likely that VEGF has important roles as a proinflammatory, a permeability-inducing, and an angiogenesis factor not only in the early inflammatory phase but also in the late fibrotic phase. Furthermore, this method may be beneficial for treating lung injury and fibrosis from the viewpoint of clinical application, since it does not require the use of a viral vector or neutralizing Ab.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
175
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1224-31
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:16002726-Animals, pubmed-meshheading:16002726-Apoptosis, pubmed-meshheading:16002726-Bleomycin, pubmed-meshheading:16002726-Bronchoalveolar Lavage Fluid, pubmed-meshheading:16002726-Cell Count, pubmed-meshheading:16002726-Cytokines, pubmed-meshheading:16002726-Disease Models, Animal, pubmed-meshheading:16002726-Extracellular Matrix Proteins, pubmed-meshheading:16002726-Gene Therapy, pubmed-meshheading:16002726-In Situ Nick-End Labeling, pubmed-meshheading:16002726-Intubation, Intratracheal, pubmed-meshheading:16002726-Kinetics, pubmed-meshheading:16002726-Lung, pubmed-meshheading:16002726-Male, pubmed-meshheading:16002726-Mice, pubmed-meshheading:16002726-Mice, Inbred C57BL, pubmed-meshheading:16002726-Myosin Heavy Chains, pubmed-meshheading:16002726-Nonmuscle Myosin Type IIB, pubmed-meshheading:16002726-Proteins, pubmed-meshheading:16002726-Pulmonary Fibrosis, pubmed-meshheading:16002726-Transfection, pubmed-meshheading:16002726-Vascular Endothelial Growth Factor A, pubmed-meshheading:16002726-Vascular Endothelial Growth Factor Receptor-1
pubmed:year
2005
pubmed:articleTitle
Anti-vascular endothelial growth factor gene therapy attenuates lung injury and fibrosis in mice.
pubmed:affiliation
Research Institute for Diseases of the Chest, Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't