Proproliferative phenotype of pulmonary microvascular endothelial cells.
Proproliferative phenotype of pulmonary microvascular endothelial cells.
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肺微血管内皮细胞的增殖表型。
DOI:
10.1152/ajplung.00304.2006
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发表时间:
2007
期刊:
影响因子:
--
通讯作者:
Fouty,Brian
中科院分区:
文献类型:
--
作者:
Solodushko,Victor;Fouty,Brian
Endothelial cells perform a number of important functions including release of vasodilators, control of the coagulation cascade, and restriction of solutes and fluid from the extravascular space. Regulation of fluid balance is of particular importance in the microcirculation of the lung where the loss of endothelial barrier function can lead to alveolar flooding and life-threatening hypoxemia. Significant heterogeneity exists between endothelial cells lining the microcirculation and cells from larger pulmonary arteries, however, and these differences may be relevant in restoring barrier function following vascular injury. Using well-defined populations of rat endothelial cells harvested from the pulmonary microcirculation [pulmonary microvascular endothelial cells (PMVEC)] and from larger pulmonary arteries [pulmonary artery endothelial cells (PAEC)], we compared their growth characteristics in low serum conditions. Withdrawal of serum inhibited proliferation and induced G0/G1arrest in PAEC, whereas PMVEC failed to undergo G0/G1arrest and continued to proliferate. Consistent with this observation, PMVEC had an increased cdk4 and cdk2 kinase activity with hyperphosphorylated (inactive) retinoblastoma (Rb) relative to PAEC as well as a threefold increase in cyclin D1 protein levels; overexpression of the cdk inhibitors p21Cip1/Waf1and p27Kip1induced G0/G1arrest. While serum withdrawal failed to induce G0/G1arrest in nonconfluent PMVEC, confluence was associated with hypophosphorylated Rb and growth arrest; loss of confluence led to resumption of growth. These data suggest that nonconfluent PMVEC continue to proliferate independently of growth factors. This proliferative characteristic may be important in restoring confluence (and barrier function) in the pulmonary microcirculation following endothelial injury.
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DOI:
10.1152/ajplung.00433.2004
发表时间:
2005
期刊:
American journal of physiology. Lung cellular and molecular physiology
影响因子:
--
作者:
Zhu,Bing;Strada,Samuel;Stevens,Troy
通讯作者:
Stevens,Troy
DOI:
--
发表时间:
2000
期刊:
Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
影响因子:
--
作者:
Grimison,B;Langan,TA;Sclafani,RA
通讯作者:
Sclafani,RA
DOI:
10.1152/ajplung.00488.2001
发表时间:
2002-12-01
影响因子:
4.9
作者:
Parker, JC;Yoshikawa, S
通讯作者:
Yoshikawa, S
DOI:
--
发表时间:
1999
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Nath,N;Bian,H;Reed,EF;Chellappan,SP
通讯作者:
Chellappan,SP
影响因子:
10.5
作者:
Diehl, JA;Cheng, MG;Sherr, CJ
通讯作者:
Sherr, CJ