Abstract:
OBJECTIVE:Pericytes, located in close proximity to the underlying endothelium, form an integral component of the microvasculature. These cells are intimately involved in angiogenesis, which is of fundamental importance in many physiological and pathological processes. We evaluated the influence of pericyte-conditioned medium (PCM) on endothelial cell growth characteristics and modulation of endothelial gene expression. METHODS:Migration and tubule formation assays were performed in vitro to determine the effect of PCM on endothelial growth characteristics. cDNA microarray analysis was used to identify alterations in gene expression following exposure of human microvascular endothelial cells (HMEC-1) to PCM. Overexpression of PAI-1 using recombinant protein or transient transfection, and inhibition using an inhibitory antibody against PAI-1, were used to determine whether up- or down-regulation of this gene was responsible for the changes in endothelial cell characteristics observed in response to PCM exposure. RESULTS:We have shown that PCM exerts a dramatic inhibitory influence on endothelial cell migration in vitro. In addition, endothelial cells cultured on Matrigel and exposed to PCM were found to generate significantly fewer angiogenic branches. Microarray analysis of endothelial cells exposed to PCM identified PAI-1 as the gene showing the greatest level of differential expression (3.4-fold induction). Studies using an inhibitory antibody to PAI-1 suggest that induction of this protein by PCM is pivotal to the observed inhibitory influence on the migratory and angiogenic potential of HMEC-1. We further investigated this by overexpressing PAI-1, which was shown to have a potent inhibitory influence on EC migration and angiogenic branching, although the concentration of PAI-1 was clearly important. CONCLUSION:Collectively, these findings suggest that PCM contains a bioactive element(s) that controls both endothelial cell migration and tubule formation in vitro and that these responses may be partially controlled by increased endothelial cell expression of PAI-1.
journal_name
Cardiovasc Resjournal_title
Cardiovascular researchauthors
McIlroy M,O'Rourke M,McKeown SR,Hirst DG,Robson Tdoi
10.1016/j.cardiores.2005.08.003subject
Has Abstractpub_date
2006-01-01 00:00:00pages
207-17issue
1eissn
0008-6363issn
1755-3245pii
S0008-6363(05)00406-2journal_volume
69pub_type
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journal_title:Cardiovascular research
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pub_type: 杂志文章,评审
doi:10.1016/j.cardiores.2007.02.029
更新日期:2007-07-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:2015-12-01 00:00:00
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pub_type: 杂志文章
doi:10.1016/s0008-6363(02)00539-4
更新日期:2002-11-01 00:00:00
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doi:10.1016/s0008-6363(97)00092-8
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更新日期:2011-01-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/s0008-6363(99)00103-0
更新日期:1999-09-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 临床试验,杂志文章
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更新日期:1997-04-01 00:00:00
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pub_type: 杂志文章,评审
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更新日期:2014-07-01 00:00:00
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更新日期:2008-09-01 00:00:00
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pub_type: 杂志文章
doi:10.1093/cvr/26.6.603
更新日期:1992-06-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1016/j.cardiores.2003.10.003
更新日期:2004-01-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/26.4.371
更新日期:1992-04-01 00:00:00
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pub_type: 杂志文章
doi:10.1093/cvr/cvr158
更新日期:2011-10-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1093/cvr/cvu264
更新日期:2015-03-01 00:00:00
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journal_title:Cardiovascular research
pub_type: 杂志文章
doi:10.1093/cvr/cvn002
更新日期:2008-05-01 00:00:00