Source:http://linkedlifedata.com/resource/pubmed/id/18568946
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2008-6-23
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| pubmed:abstractText |
Overexpression of a caspase-resistant form of Bcl-2 (D34A) in human umbilical vein endothelial cells (ECs) implanted into immunodeficient mice promotes the maturation of human EC-lined microvessels invested by vascular smooth muscle cells (VSMCs) of mouse origin. In contrast, EC implants not overexpressing Bcl-2 form only simple, uncoated EC tubes. Here the authors compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of EC expressing different forms of Bcl-2. Wild-type Bcl-2, like the caspase-resistant D34A Bcl-2 mutant, is antiapoptotic in vitro and promotes VSMC recruitment in vivo, whereas a G145E mutant that has diminished antiapoptotic activity in vitro does not promote vessel maturation in vivo. The D34A and wild-type forms of Bcl-2, but not the G145E mutant form of Bcl-2, significantly regulate RNA transcripts previously associated with EC-VSMC interactions and VSMC biology, including matrix Gla protein, insulin-like growth factor-binding protein (IGFBP)-2, matrix metalloproteinase (MMP)-14, ADAM17, stanniocalcin-1, and targets of the nuclear factor (NF)-kappa B, cAMP response element-binding (CREB), and activator protein 1 (AP1) transcription factor families. These effects of Bcl-2 on the transcriptome are detected in ECs cultured as angiogenic three-dimensional (3-D) tubes but are attenuated in ECs cultured as 2-D monolayers. Bcl-2-regulated transcription in ECs may contribute to vascular maturation, and support design of tissue engineering strategies using EC.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
1029-2373
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
15
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
59-71
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| pubmed:meshHeading |
pubmed-meshheading:18568946-Animals,
pubmed-meshheading:18568946-Apoptosis,
pubmed-meshheading:18568946-Blood Vessels,
pubmed-meshheading:18568946-Cell Culture Techniques,
pubmed-meshheading:18568946-Cells, Cultured,
pubmed-meshheading:18568946-Endothelial Cells,
pubmed-meshheading:18568946-Endothelium, Vascular,
pubmed-meshheading:18568946-Humans,
pubmed-meshheading:18568946-Immunohistochemistry,
pubmed-meshheading:18568946-Mice,
pubmed-meshheading:18568946-Mice, SCID,
pubmed-meshheading:18568946-Models, Genetic,
pubmed-meshheading:18568946-Muscle, Smooth, Vascular,
pubmed-meshheading:18568946-Mutation,
pubmed-meshheading:18568946-Organ Culture Techniques,
pubmed-meshheading:18568946-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:18568946-Retroviridae,
pubmed-meshheading:18568946-Transcription, Genetic,
pubmed-meshheading:18568946-Transduction, Genetic,
pubmed-meshheading:18568946-Transfection,
pubmed-meshheading:18568946-Transplantation, Heterologous,
pubmed-meshheading:18568946-Umbilical Veins
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| pubmed:articleTitle |
Antiapoptotic activities of bcl-2 correlate with vascular maturation and transcriptional modulation of human endothelial cells.
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| pubmed:affiliation |
Department of Pathology, Yale University School of Medicine, New Haven, Connecticut, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|