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黏着斑激酶对细胞群体力学行为的影响。

Influence of focal adhesion kinase on the mechanical behavior of cell populations.

机构信息

Center for Medical Physics and Technology, Biophysics Group, Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Germany.

出版信息

Biochem Biophys Res Commun. 2013 Jun 28;436(2):246-51. doi: 10.1016/j.bbrc.2013.05.084. Epub 2013 May 30.

DOI:10.1016/j.bbrc.2013.05.084
PMID:23726908
Abstract

Mechanical forces play an important role in the organization, growth, maturation, and function of living tissues. At the cellular level, the transmission of forces from outside the cell through cell-matrix and cell-cell contacts are believed to control spreading, motility, maturation as well as intracellular signaling cascades that may change many characteristics in cells. We looked at cell populations of mouse embryonic fibroblasts that are deficient of focal adhesion kinase (FAK) and examined their mechanical profile. We observed that the lack of FAK induces a mesenchymal-epithelial switch including the regulation of adherens junctions via E-cadherin, leading to increased cell-cell-cohesion. Our results show that the absence of FAK influences the macroscopic cell colony spreading in two (2D) and three (3D) dimensions as well as the velocity fields of the tissue, the single cell persistence and correlation length, changing from an independent to a collective mode of migration. Additionally, the single cell size in the sheet decreases significantly.

摘要

机械力在组织、生长、成熟和活体组织功能中起着重要作用。在细胞水平上,细胞外的力通过细胞基质和细胞-细胞接触传递,被认为可以控制细胞的扩展、运动、成熟以及可能改变细胞许多特性的细胞内信号级联。我们观察了缺乏粘着斑激酶 (FAK) 的小鼠胚胎成纤维细胞群体,并检查了它们的力学特征。我们发现,缺乏 FAK 会诱导上皮-间充质转化,包括通过 E-钙粘蛋白调节粘着连接,从而增加细胞间的黏附。我们的结果表明,FAK 的缺失会影响二维 (2D) 和三维 (3D) 宏观细胞集落的扩展,以及组织的速度场、单个细胞的持久性和相关长度,从独立模式向集体模式迁移。此外,薄片中的单个细胞尺寸显著减小。

相似文献

1
Influence of focal adhesion kinase on the mechanical behavior of cell populations.黏着斑激酶对细胞群体力学行为的影响。
Biochem Biophys Res Commun. 2013 Jun 28;436(2):246-51. doi: 10.1016/j.bbrc.2013.05.084. Epub 2013 May 30.
2
Dynamic conformational changes in the FERM domain of FAK are involved in focal-adhesion behavior during cell spreading and motility.粘着斑激酶(FAK)的FERM结构域中的动态构象变化参与细胞铺展和运动过程中的粘着斑行为。
J Cell Sci. 2009 Mar 1;122(Pt 5):656-66. doi: 10.1242/jcs.028738. Epub 2009 Feb 10.
3
Reduced cell motility and enhanced focal adhesion contact formation in cells from FAK-deficient mice.FAK基因缺陷小鼠细胞的细胞运动性降低,粘着斑接触形成增强。
Nature. 1995 Oct 12;377(6549):539-44. doi: 10.1038/377539a0.
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Src and FAK signalling controls adhesion fate and the epithelial-to-mesenchymal transition.Src和粘着斑激酶信号传导控制粘附命运以及上皮-间质转化。
Curr Opin Cell Biol. 2005 Oct;17(5):542-7. doi: 10.1016/j.ceb.2005.08.007.
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TGFbeta-induced EMT requires focal adhesion kinase (FAK) signaling.转化生长因子β诱导的上皮-间质转化需要粘着斑激酶(FAK)信号传导。
Exp Cell Res. 2008 Jan 1;314(1):143-52. doi: 10.1016/j.yexcr.2007.09.005. Epub 2007 Sep 18.
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FAK promotes organization of fibronectin matrix and fibrillar adhesions.黏着斑激酶促进纤连蛋白基质的组织形成和纤维状黏附。
J Cell Sci. 2004 Jan 15;117(Pt 2):177-87. doi: 10.1242/jcs.00845. Epub 2003 Dec 2.
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[Morphology, cell-cell interactions, and migratory activity of IAR-2 epithelial cells transformed with the RAS oncogene: contribution of cell adhesion protein E-cadherin].[用RAS癌基因转化的IAR-2上皮细胞的形态学、细胞间相互作用及迁移活性:细胞粘附蛋白E-钙粘蛋白的作用]
Ontogenez. 2011 Nov-Dec;42(6):453-64.
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The tyrosine phosphatase DEP-1 induces cytoskeletal rearrangements, aberrant cell-substratum interactions and a reduction in cell proliferation.酪氨酸磷酸酶DEP-1可诱导细胞骨架重排、异常的细胞与基质相互作用以及细胞增殖减少。
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Traction forces exerted through N-cadherin contacts.通过N-钙黏着蛋白接触产生的牵引力。
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FAK phosphorylation at Ser-843 inhibits Tyr-397 phosphorylation, cell spreading and migration.粘着斑激酶(FAK)在丝氨酸843位点的磷酸化抑制酪氨酸397位点的磷酸化、细胞铺展和迁移。
J Cell Physiol. 2007 Feb;210(2):436-44. doi: 10.1002/jcp.20870.

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