Source:http://linkedlifedata.com/resource/pubmed/id/19901963
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2010-2-11
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pubmed:abstractText |
The Capillary Morphogenesis Gene 2 (CMG2) gene encodes an Anthrax toxin receptor (ANTXR2), but the normal physiological function is not known. ANTXR2/CMG2 was originally identified as a result of up-regulation during capillary morphogenesis of endothelial cells (ECs) cultured in vitro. We explored the hypothesis that key steps of the angiogenic process are either dependent or are influenced by ANTXR2/CMG2 activity. We describe the expression pattern of ANTXR2/CMG2 in several murine tissues and in normal breast and breast tumors. Endothelial expression was found in all of the tissues analyzed, in cultured ECs and in breast tumor vessels; however, ANTXR2/CMG2 expression was not restricted to this cell type. To assess potential angiogenic function, we used RNA interference to achieve significant reduction of ANTXR2/CMG2 expression in cultured human umbilical venous endothelial cells (HUVECs). Reduced ANTXR2/CMG2 expression resulted in significant inhibition of proliferation and reduced capacity of ECs to form capillary-like networks in vitro, whereas overexpression of ANTXR2/CMG2 in HUVEC increased proliferation and capillary-like network formation. Little change in migration of ECs was observed on knockdown or overexpression. We conclude that ANTXR2/CMG2 functions to promote endothelial proliferation and morphogenesis during sprouting angiogenesis, consistent with the endothelial expression of ANTXR2/CMG2 in several vascular beds.
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pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/AI48489,
http://linkedlifedata.com/resource/pubmed/grant/DK07328,
http://linkedlifedata.com/resource/pubmed/grant/NIH RO1 AI064654,
http://linkedlifedata.com/resource/pubmed/grant/NIH RO1 HL62454,
http://linkedlifedata.com/resource/pubmed/grant/R01 AI064654-04,
http://linkedlifedata.com/resource/pubmed/grant/R01 AI064654-05,
http://linkedlifedata.com/resource/pubmed/grant/R01 AI076852-02
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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:month |
Feb
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pubmed:issn |
1476-5594
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
11
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pubmed:volume |
29
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
789-801
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pubmed:dateRevised |
2011-11-9
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pubmed:meshHeading |
pubmed-meshheading:19901963-Animals,
pubmed-meshheading:19901963-Breast,
pubmed-meshheading:19901963-Capillaries,
pubmed-meshheading:19901963-Cell Line,
pubmed-meshheading:19901963-Cell Movement,
pubmed-meshheading:19901963-Cell Proliferation,
pubmed-meshheading:19901963-Endothelial Cells,
pubmed-meshheading:19901963-Endothelium,
pubmed-meshheading:19901963-Gene Expression Regulation,
pubmed-meshheading:19901963-Gene Knockdown Techniques,
pubmed-meshheading:19901963-Humans,
pubmed-meshheading:19901963-Immunohistochemistry,
pubmed-meshheading:19901963-Mice,
pubmed-meshheading:19901963-Mice, Inbred C57BL,
pubmed-meshheading:19901963-Morphogenesis,
pubmed-meshheading:19901963-Neoplasms,
pubmed-meshheading:19901963-Neovascularization, Physiologic,
pubmed-meshheading:19901963-Receptors, Peptide
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pubmed:year |
2010
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pubmed:articleTitle |
Anthrax toxin receptor 2 is expressed in murine and tumor vasculature and functions in endothelial proliferation and morphogenesis.
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pubmed:affiliation |
Columbia University Medical Center, New York, NY 10035, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, N.I.H., Extramural
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