scholarly journals Lipid phosphatases SKIP and SHIP 2 regulate fibronectin‐dependent cell migration in glioblastoma

FEBS Journal ◽  
2019 ◽  
Vol 286 (6) ◽  
pp. 1120-1135 ◽  
Author(s):  
Ana Raquel Ramos ◽  
Somadri Ghosh ◽  
Matthias Dedobbeleer ◽  
Pierre A. Robe ◽  
Bernard Rogister ◽  
...  
Keyword(s):  
Cell Migration ◽  
Lipid Phosphatases ◽  
Dependent Cell

Urokinase-receptor-mediated phenotypic changes in vascular smooth muscle cells require the involvement of membrane rafts

2009 ◽  
Vol 423 (3) ◽  
pp. 343-351 ◽  
Author(s):  
Julia Kiyan ◽  
Graham Smith ◽  
Hermann Haller ◽  
Inna Dumler
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Lipid Rafts ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Caveolin 1 ◽  
Phenotypic Changes ◽  
Dependent Cell

The cholesterol-enriched membrane microdomains lipid rafts play a key role in cell activation by recruiting and excluding specific signalling components of cell-surface receptors upon receptor engagement. Our previous studies have demonstrated that the GPI (glycosylphosphatidylinositol)-linked uPAR [uPA (urokinase-type plasminogen activator) receptor], which can be found in lipid rafts and in non-raft fractions, can mediate the differentiation of VSMCs (vascular smooth muscle cells) towards a pathophysiological de-differentiated phenotype. However, the mechanism by which uPAR and its ligand uPA regulate VSMC phenotypic changes is not known. In the present study, we provide evidence that the molecular machinery of uPAR-mediated VSMC differentiation employs lipid rafts. We show that the disruption of rafts in VSMCs by membrane cholesterol depletion using MCD (methyl-β-cyclodextrin) or filipin leads to the up-regulation of uPAR and cell de-differentiation. uPAR silencing by means of interfering RNA resulted in an increased expression of contractile proteins. Consequently, disruption of lipid rafts impaired the expression of these proteins and transcriptional activity of related genes. We provide evidence that this effect was mediated by uPAR. Similar effects were observed in VSMCs isolated from Cav1−/− (caveolin-1-deficient) mice. Despite the level of uPAR being significantly higher after the disruption of the rafts, uPA/uPAR-dependent cell migration was impaired. However, caveolin-1 deficiency impaired only uPAR-dependent cell proliferation, whereas cell migration was strongly up-regulated in these cells. Our results provide evidence that rafts are required in the regulation of uPAR-mediated VSMC phenotypic modulations. These findings suggest further that, in the context of uPA/uPAR-dependent processes, caveolae-associated and non-associated rafts represent different signalling membrane domains.

Complexes of tetraspanins with integrins: more than meets the eye

2001 ◽  
Vol 114 (23) ◽  
pp. 4143-4151 ◽  
Author(s):  
Fedor Berditchevski
Keyword(s):  
Cell Migration ◽  
Distinct Type ◽  
Cell Periphery ◽  
Diverse Range ◽  
Kinase C ◽  
Biological Phenomena ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Dependent Cell ◽  
Phosphatidylinositol 4

The transmembrane proteins of the tetraspanin superfamily are implicated in a diverse range of biological phenomena, including cell motility, metastasis, cell proliferation and differentiation. The tetraspanins are associated with adhesion receptors of the integrin family and regulate integrin-dependent cell migration. In cells attached to the extracellular matrix, the integrin-tetraspanin adhesion complexes are clustered into a distinct type of adhesion structure at the cell periphery. Various tetraspanins are associated with phosphatidylinositol 4-kinase and protein kinase C isoforms, and they may facilitate assembly of signalling complexes by tethering these enzymes to integrin heterodimers. At the plasma membrane, integrin-tetraspanin signalling complexes are partitioned into specific microdomains proximal to cholesterol-rich lipid rafts. A substantial fraction of tetraspanins colocalise with integrins in various intracellular vesicular compartments. It is proposed that tetraspanins can influence cell migration by one of the following mechanisms: (1) modulation of integrin signalling; (2) compartmentalisation of integrins on the cell surface; or (3) direction of intracellular trafficking and recycling of integrins.

Analysis of Matrix-Dependent Cell Migration with a Barrier Migration Assay

2010 ◽  
Vol 3 (126) ◽  
pp. pl1-pl1 ◽  
Author(s):  
S. Kroening ◽  
M. Goppelt-Struebe
Keyword(s):  
Cell Migration ◽  
Migration Assay ◽  
Dependent Cell

Activation of IP and EP3 receptors alters cAMP-dependent cell migration

2002 ◽  
Vol 444 (1-2) ◽  
pp. 31-37 ◽  
Author(s):  
Rüdiger Blindt ◽  
Anja-K. Bosserhoff ◽  
Jürgen vom Dahl ◽  
Peter Hanrath ◽  
Karsten Schrör ◽  
...  
Keyword(s):  
Cell Migration ◽  
Dependent Cell

scholarly journals Evidence for a role of glycosphingolipids in CXCR4-dependent cell migration

FEBS Letters ◽  
2007 ◽  
Vol 581 (14) ◽  
pp. 2641-2646 ◽  
Author(s):  
Cristina Limatola ◽  
Valeria Massa ◽  
Clotilde Lauro ◽  
Myriam Catalano ◽  
Anna Giovanetti ◽  
...  
Keyword(s):  
Cell Migration ◽  
Dependent Cell

Spatiotemporally-regulated interaction between β1 integrin and ErbB4 that is involved in fibronectin-dependent cell migration

2011 ◽  
Vol 149 (3) ◽  
pp. 347-355 ◽  
Author(s):  
Ryusuke Yamashita ◽  
Norihiro Kotani ◽  
Yoshihito Ishiura ◽  
Shigeki Higashiyama ◽  
Koichi Honke
Keyword(s):  
Cell Migration ◽  
Β1 Integrin ◽  
Dependent Cell
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