Human microvascular endothelial cells adhere to thrombospondin-1 via an RGD/CSVTCG domain independent mechanism.

Human microvascular endothelial cells adhere to thrombospondin-1 via an RGD/CSVTCG domain independent mechanism.
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人微血管内皮细胞通过 RGD/CSVTCG 结构域独立机制粘附到血小板反应蛋白-1。

DOI:
10.1111/1523-1747.ep12340475
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发表时间:
1996
期刊:
The Journal of investigative dermatology
影响因子:
--
通讯作者:
Swerlick,RA
Swerlick,RA
中科院分区:
--
文献类型:
--
作者:
Chen,ZS;Pohl,J;Lawley,TJ;Swerlick,RA

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Thrombospondin-1 (TSP-1), a 450-kDa glycoprotein secreted by platelets and endothelial cells at sites of tissue injury or inflammation, plays an important role in angiogenesis, inflammation, and vascular occlusive skin diseases. Many of the physiologic and pathologic activities of TSP-1 are dependent upon its interactions with endothelial cells. To better understand the basis of these activities, we examined the mechanisms mediating the binding of human dermal microvascnlar endothelial cells (HDMEC) to immobilized TSP-1. HDMEC bound to but did not spread on TSP-1 in a concentration-dependent manner. Monoclonal antibodies (MoAbs) which recognize two purported TSP-1 binding proteins, CD36 and theαv integrin chain, or TSP-l-derived peptides CGRGDS and CSVTCG, alone or in combination with heparin, did not inhibit HDMEC adhesion to immobilized TSP-1. Furthermore, CSVTCG-ovalbumin conjugates failed to support HDMEC adhesion. Although RGD-containing peptides immobilized on plastic wells supported HDMEC binding, they also induced cell spreading not characteristic of cell binding to TSP-1 and binding was inhibited by free RGD peptide. Two MoAbs against different domains of TSP-1 (A4.1 and C6.1) failed to block HDMEC binding to TSP-1, but both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%. Acid treatment of TSP-1 almost completely abrogated its ability to support HDMEC binding, while acid treatment inhibited G361 binding by 50%. However, either antibody completely abrogated G-361 cell binding to acid-treated TSP-1. These data demonstrate that HDMEC bind to immobilized TSP-1 in an RGD- and CSVTCG-independent manner via an acid labile epitope(s) which is recognized via a receptor or receptors distinct from CD36 orαvβintegrin receptor.
细胞附着血小板反应蛋白的多种机制。
DOI: 10.1242/jcs.104.4.1061
发表时间: 1993
影响因子: 4
作者:
Adams,JC;Lawler,J
通讯作者: Lawler,J
内皮细胞血小板反应蛋白的细胞结合域:定位到 70-kDa 核心片段并确定结合特性。
DOI: --
发表时间: 1991
期刊: Biochemistry
影响因子: 2.9
作者:
R. Dardik;J. Lahav
通讯作者: J. Lahav
DOI: 10.1016/s0021-9258(18)43930-0
发表时间: 1994-11
期刊: The Journal of biological chemistry
影响因子: --
作者:
A. Gao;W. Frazier
通讯作者: A. Gao;W. Frazier
DOI: 10.1126/science.7521539
发表时间: 1994-09-09
期刊: SCIENCE
影响因子: 56.9
作者:
DAMERON, KM;VOLPERT, OV;BOUCK, N
通讯作者: BOUCK, N
血小板反应蛋白与血小板糖蛋白 GPIIb-IIIa 的相互作用。
DOI: --
发表时间: 1989
期刊: The Journal of biological chemistry
影响因子: --
作者:
Karczewski,J;Knudsen,KA;Smith,L;Murphy,A;Rothman,VL;Tuszynski,GP
通讯作者: Tuszynski,GP