Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-7-4
pubmed:abstractText
Endostatin is a cleavage product of collagen XVIII that inhibits tumor angiogenesis and growth. Interferon alpha2a blocks tumor angiogenesis and causes regression of hemangiomas, but has no effect on choroidal neovascularization (CNV). Therefore, inhibitors of tumor angiogenesis do not necessarily inhibit ocular neovascularization. In this study, we used an intravenous injection of adenoviral vectors containing a sig-mEndo transgene consisting of murine immunoglobulin kappa-chain leader sequence coupled to sequence coding for murine endostatin to investigate the effect of high serum levels of endostatin on CNV in mice. Mice injected with a construct in which sig-mEndo expression was driven by the Rous sarcoma virus promoter had moderately high serum levels of endostatin and significantly smaller CNV lesions at sites of laser-induced rupture of Bruch's membrane than mice injected with null vector. Mice injected with a construct in which sig-mEndo was driven by the simian cytomegalovirus promoter had approximately 10-fold higher endostatin serum levels and had nearly complete prevention of CNV. There was a strong inverse correlation between endostatin serum level and area of CNV. This study provides proof of principle that gene therapy to increase levels of endostatin can prevent the development of CNV and may provide a new treatment for the leading cause of severe loss of vision in patients with age-related macular degeneration.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-10362799, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-10398599, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-10416583, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-10489375, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-10536005, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-10749112, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-10758166, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-10765935, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-10967078, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-11020798, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-11040088, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-11193216, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-1489383, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-1688470, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-1697685, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-1714270, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-2152815, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-2464438, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-2734305, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-3543687, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-7517405, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-7525077, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-7679482, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-8258518, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-8892868, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-9008168, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-9230826, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-9430560, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-9759925, http://linkedlifedata.com/resource/pubmed/commentcorrection/11438478-9811357
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0002-9440
pubmed:author
pubmed:issnType
Print
pubmed:volume
159
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
313-20
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:11438478-Adenoviridae, pubmed-meshheading:11438478-Angiogenesis Inhibitors, pubmed-meshheading:11438478-Animals, pubmed-meshheading:11438478-Choroid, pubmed-meshheading:11438478-Collagen, pubmed-meshheading:11438478-Collagen Type XVIII, pubmed-meshheading:11438478-Endostatins, pubmed-meshheading:11438478-Gene Expression, pubmed-meshheading:11438478-Gene Therapy, pubmed-meshheading:11438478-Genes, Reporter, pubmed-meshheading:11438478-Genetic Vectors, pubmed-meshheading:11438478-Injections, Intravenous, pubmed-meshheading:11438478-Liver, pubmed-meshheading:11438478-Mice, pubmed-meshheading:11438478-Mice, Inbred C57BL, pubmed-meshheading:11438478-Neovascularization, Pathologic, pubmed-meshheading:11438478-Ocular Physiological Phenomena, pubmed-meshheading:11438478-Peptide Fragments, pubmed-meshheading:11438478-Recombination, Genetic
pubmed:year
2001
pubmed:articleTitle
Inhibition of choroidal neovascularization by intravenous injection of adenoviral vectors expressing secretable endostatin.
pubmed:affiliation
Department of Ophthalmology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287-9277, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't