Abstract:
:Junction dynamics of endothelial cells are based on the integration of signal transduction, cytoskeletal remodeling and contraction, which are necessary for the formation and maintenance of monolayer integrity, but also enable repair and regeneration. The VE-cadherin-catenin complex forms the molecular basis of the adherence junctions and cooperates closely with actin filaments. Several groups have recently described small actin-driven protrusions at the cell junctions that are controlled by the Arp2/3 complex, contributing to cell junction regulation. We identified these protrusions as the driving force for VE-cadherin dynamics, as they directly induce new VE-cadherin-mediated adhesion sites, and have accordingly referred to these structures as junction-associated intermittent lamellipodia (JAIL). JAIL extend over only a few microns and thus provide the basis for a subcellular regulation of adhesion. The local (subcellular) VE-cadherin concentration and JAIL formation are directly interdependent, which enables autoregulation. Therefore, this mechanism can contribute a subcellularly regulated adaptation of cell contact dynamics, and is therefore of great importance for monolayer integrity and relative cell migration during wound healing and angiogenesis, as well as for inflammatory responses. In this Review, we discuss the mechanisms and functions underlying these actin-driven protrusions and consider their contribution to the dynamic regulation of endothelial cell junctions.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Cao J,Schnittler Hdoi
10.1242/jcs.222893subject
Has Abstractpub_date
2019-01-03 00:00:00issue
1eissn
0021-9533issn
1477-9137pii
132/1/jcs222893journal_volume
132pub_type
杂志文章,评审abstract::The Sendai virus-induced fusion of HeLa cells has been studied by freeze-fracture electron microscopy. Freeze-fracture observations confirm previous scanning electron-microscope studies (1977) and show that at 4 degrees C virus particles bind to the cell surface and that cell agglutination results from the crosslinkin...
journal_title:Journal of cell science
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abstract::Glutathione (GSH) levels progressively decline during aging and in neurodegenerative disorders. However, the contribution of such event in mediating neuronal cell death is still uncertain. In this report, we show that, in neuroblastoma cells as well as in primary mouse cortical neurons, GSH decrease, induced by buthio...
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journal_title:Journal of cell science
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更新日期:2013-09-15 00:00:00
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journal_title:Journal of cell science
pub_type: 杂志文章
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更新日期:1999-12-01 00:00:00
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pub_type: 杂志文章
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更新日期:2020-06-22 00:00:00
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journal_title:Journal of cell science
pub_type: 杂志文章
doi:
更新日期:2000-07-01 00:00:00
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pub_type: 杂志文章
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更新日期:1991-10-01 00:00:00
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journal_title:Journal of cell science
pub_type: 杂志文章
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更新日期:2018-09-20 00:00:00
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journal_title:Journal of cell science
pub_type: 杂志文章
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更新日期:2010-11-15 00:00:00
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journal_title:Journal of cell science
pub_type: 杂志文章
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更新日期:2008-07-01 00:00:00
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doi:
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journal_title:Journal of cell science
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