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| Status |
Public on Mar 05, 2008 |
| Title |
Bcl2-induced vascular maturation |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by array
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| Summary |
Overexpression of a caspase-resistant form of Bcl-2 (D34A) in human umbilical vein endothelial cells (EC) implanted into immunodeficient mice promotes the maturation of human EC-lined microvessels invested by vascular smooth muscle cells (VSMC) of mouse origin. In contrast, EC implants not overexpressing Bcl-2 form only simple, uncoated EC tubes. Here we 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 anti-apoptotic in vitro and promotes VSMC recruitment in vivo, whereas a G145E mutant that has diminished anti-apoptotic 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 metaloproteinase-14 (MMP14), ADAM17 and Stanniocalcin-1. These effects of Bcl-2 on the transcriptome are detected in EC cultured as angiogenic 3-D tubes but are attenuated in EC cultured as 2-D monolayers. Bcl-2-regulated transcription in EC may contribute to vascular maturation, and support design of tissue engineering strategies using EC.
Keywords: genetic modification, growth condition modification.
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| Overall design |
This study consists of the analysis of human umbilical vein endothelial cells (HUVEC) cultured under several conditions, including retroviral transduction, as well as on different culture substrates and in different geometries. For a full description please see our paper in the journal Endothelium, 2008. For
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| Contributor(s) |
Print CG |
| Citation(s) |
18568946 |
| Submission date |
Mar 04, 2008 |
| Last update date |
Dec 13, 2018 |
| Contact name |
Cris Print |
| E-mail(s) |
c.print@auckland.ac.nz
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| Organization name |
Auckland University
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| Street address |
Grafton Campus, Park Rd
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| City |
Auckland |
| ZIP/Postal code |
1 |
| Country |
New Zealand |
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| Platforms (1) |
| GPL8300 |
[HG_U95Av2] Affymetrix Human Genome U95 Version 2 Array |
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| Samples (20)
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| GSM270737 |
high titre virus wild type Bcl-2 (1866) |
| GSM270738 |
high titre virus wild type Bcl-2 (1868) |
| GSM270739 |
high titre virus G145E mutant Bcl-2 (1867) |
| GSM270740 |
high titre virus G145E mutant Bcl-2 (1869) |
| GSM270741 |
high titre virus wild type Bcl-2 (1870) |
| GSM270742 |
high titre virus wild type Bcl-2 (1871) |
| GSM270743 |
high titre virus wild type Bcl-2 (1872) |
| GSM270744 |
transduced with caspase-resistant Bcl-2 (934) |
| GSM270745 |
transduced with caspase-resistant Bcl-2 (936) |
| GSM270746 |
transduced with caspase-resistant Bcl-2 (1129) |
| GSM270747 |
transduced with caspase-resistant Bcl-2 (1131) |
| GSM270748 |
transduced with eGFP (935) |
| GSM270749 |
transduced with eGFP (937) |
| GSM270750 |
transduced with eGFP (1132) |
| GSM270751 |
untransduced (1123) |
| GSM270752 |
transduced with eGFP (1126) |
| GSM270753 |
transduced with eGFP (1127) |
| GSM270754 |
transduced with caspase-resistant Bcl-2 (1133) |
| GSM270755 |
transduced with caspase-resistant Bcl-2 (1124) |
| GSM270756 |
transduced with caspase-resistant Bcl-2 (938) |
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| Relations |
| BioProject |
PRJNA107589 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE10710_RAW.tar |
55.4 Mb |
(http)(custom) |
TAR (of CEL) |
| Processed data included within Sample table |
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