scholarly journals Cell–matrix interaction via CD44 is independently regulated by different metalloproteinases activated in response to extracellular Ca2+ influx and PKC activation

2004 ◽  
Vol 165 (6) ◽  
pp. 893-902 ◽  
Author(s):  
Osamu Nagano ◽  
Daizo Murakami ◽  
Dieter Hartmann ◽  
Bart de Strooper ◽  
Paul Saftig ◽  
...  
Keyword(s):  
Cell Migration ◽  
Small Gtpase ◽  
Temporal Regulation ◽  
Matrix Interaction ◽  
Cell Matrix ◽  
Kinase C ◽  
Spatio Temporal ◽  
Proteolytic Cleavages ◽  
Cell Matrix Adhesion ◽  
Pkc Activation

CD44 is an adhesion molecule that interacts with hyaluronic acid (HA) and undergoes sequential proteolytic cleavages in its ectodomain and intramembranous domain. The ectodomain cleavage is triggered by extracellular Ca2+ influx or the activation of protein kinase C. Here we show that CD44-mediated cell–matrix adhesion is terminated by two independent ADAM family metalloproteinases, ADAM10 and ADAM17, differentially regulated in response to those stimuli. Ca2+ influx activates ADAM10 by regulating the association between calmodulin and ADAM10, leading to CD44 ectodomain cleavage. Depletion of ADAM10 strongly inhibits the Ca2+ influx-induced cell detachment from matrix. On the other hand, phorbol ester stimulation activates ADAM17 through the activation of PKC and small GTPase Rac, inducing proteolysis of CD44. Furthermore, depletion of ADAM10 or ADAM17 markedly suppressed CD44-dependent cancer cell migration on HA, but not on fibronectin. The spatio-temporal regulation of two independent signaling pathways for CD44 cleavage plays a crucial role in cell–matrix interaction and cell migration.

Cell–matrix adhesion complexes: Master control machinery of cell migration

2008 ◽  
Vol 18 (1) ◽  
pp. 65-76 ◽  
Author(s):  
John G. Lock ◽  
Bernhard Wehrle-Haller ◽  
Staffan Strömblad
Keyword(s):  
Cell Migration ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Master Control

scholarly journals Supracellular organization confers directionality and mechanical potency to migrating pairs of cardiopharyngeal progenitor cells

2021 ◽  
Author(s):  
Yelena Y. Bernadskaya ◽  
Haicen Yue ◽  
Calina Copos ◽  
Lionel Christiaen ◽  
Alex Mogilner
Keyword(s):  
Cell Migration ◽  
Cell Communication ◽  
Biomechanical Properties ◽  
Collective Cell Migration ◽  
Cellular Potts Model ◽  
Cellular Mechanics ◽  
Cell Matrix ◽  
Collective Movements ◽  
Cell Matrix Adhesion

AbstractPhysiological and pathological morphogenetic events involve a wide array of collective movements, suggesting that these multicellular arrangements confer biochemical and biomechanical properties that contribute to tissue scale organization. The cardiopharyngeal progenitors of the tunicate Ciona provide the simplest possible model of collective cell migration. They form cohesive bilateral cell pairs, leader-trailer polarized along the migration path as they migrate between the ventral epidermis and trunk endoderm. Here, circumventing difficulties in quantifying cellular mechanics in live embryos, we use the Cellular Potts Model to computationally probe the distributions of forces consistent with the shapes and collective polarity of migrating cell pairs. Combining computational modeling, confocal microscopy, and molecular perturbations, we first determine that cardiopharyngeal progenitors display hallmarks of supracellular organization, with differential distributions of protrusive forces, cell-matrix adhesion, and myosin-based retraction forces along the leader-trailer axis. Combined 4D simulations and experimental observations suggest that cell-cell communication helps establish a hierarchy that contributes to aligning collective polarity with the direction of migration, as observed with three or more cells both in silico and in vivo. Our approach reveals emerging properties of the migrating collective. Specifically, cell pairs are more persistent, thus migrating over longer distances, and presumably with higher accuracy. Finally, simulations suggest that polarized cell pairs literally join forces to deform the trunk endoderm, as they migrate through the extracellular space. We thus propose that the polarized supracellular organization of cardiopharyngeal progenitors confers emergent physical properties that determine mechanical interactions with their environment during morphogenesis.

scholarly journals Ca2+/H+ exchange by acidic organelles regulates cell migration in vivo

2016 ◽  
Vol 212 (7) ◽  
pp. 803-813 ◽  
Author(s):  
Manuela Melchionda ◽  
Jon K. Pittman ◽  
Roberto Mayor ◽  
Sandip Patel
Keyword(s):  
Cell Migration ◽  
Neural Crest ◽  
Cell Matrix ◽  
Physiological Relevance ◽  
Underlying Mechanisms ◽  
Acidic Organelles ◽  
Cell Matrix Adhesion ◽  
Insight Into

Increasing evidence implicates Ca2+ in the control of cell migration. However, the underlying mechanisms are incompletely understood. Acidic Ca2+ stores are fast emerging as signaling centers. But how Ca2+ is taken up by these organelles in metazoans and the physiological relevance for migration is unclear. Here, we identify a vertebrate Ca2+/H+ exchanger (CAX) as part of a widespread family of homologues in animals. CAX is expressed in neural crest cells and required for their migration in vivo. It localizes to acidic organelles, tempers evoked Ca2+ signals, and regulates cell-matrix adhesion during migration. Our data provide new molecular insight into how Ca2+ is handled by acidic organelles and link this to migration, thereby underscoring the role of noncanonical Ca2+ stores in the control of Ca2+-dependent function.

scholarly journals The protein-tyrosine phosphatase DEP-1 modulates growth factor-stimulated cell migration and cell–matrix adhesion

Oncogene ◽  
2003 ◽  
Vol 22 (27) ◽  
pp. 4175-4185 ◽  
Author(s):  
Enrico Jandt ◽  
Karsten Denner ◽  
Marina Kovalenko ◽  
Arne Östman ◽  
Frank-D Böhmer
Keyword(s):  
Cell Migration ◽  
Growth Factor ◽  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Protein Tyrosine ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion

scholarly journals RAP1-RAC1 Signaling Has an Important Role in Adhesion and Migration in HNSCC

2020 ◽  
Vol 99 (8) ◽  
pp. 959-968 ◽  
Author(s):  
M. Liu ◽  
R. Banerjee ◽  
C. Rossa ◽  
N.J. D’Silva
Keyword(s):  
Cell Migration ◽  
Cell Adhesion ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
And Migration ◽  
Rap1 Activation ◽  
Cell Matrix Adhesion ◽  
Α5β1 Integrin ◽  
Hnscc Cell ◽  
Cell Cell

Cell-cell adhesion is a key mechanism to control tissue integrity and migration. In head and neck squamous cell carcinoma (HNSCC), cell migration facilitates distant metastases and is correlated with poor prognosis. RAP1, a ras-like protein, has an important role in the progression of HNSCC. RAC1 is an integrin-linked, ras-like protein that promotes cell migration. Here we show that loss of cell-cell adhesion is correlated with inactivation of RAP1 confirmed by 2 different biochemical approaches. RAP1 activation is required for cell-matrix adhesion confirmed by adhesion to fibronectin-coated plates with cells that have biochemically activated RAP1. This effect is reversed when RAP1 is inactivated. In addition, RAP1GTP-mediated adhesion is only facilitated through α5β1 integrin complex and is not a function of either α5 or β1 integrin alone. Moreover, the inside-out signaling of RAP1 activation is coordinated with RAC1 activation. These findings show that RAP1 has a prominent role in cell-matrix adhesion via extracellular matrix molecule fibronectin-induced α5β1 integrin and supports a critical role for the RAP1/RAC1 signaling axis in HNSCC cell migration.

scholarly journals Increased Cell-Matrix Adhesion upon Constitutive Activation of Rho Proteins by Cytotoxic Necrotizing Factors from E. coli and Y. pseudotuberculosis

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Martin May ◽  
Tanja Kolbe ◽  
Tianbang Wang ◽  
Gudula Schmidt ◽  
Harald Genth
Keyword(s):  
Cell Migration ◽  
Hela Cells ◽  
Adherent Cells ◽  
Rho Proteins ◽  
E Coli ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Established Cell ◽  
Cell Matrix Adhesion ◽  
Suspended Cells

Cytotoxic necrotizing factors (CNFs) encompass a class of autotransporter toxins produced by uropathogenic E. coli (CNF1) or Y. pseudotuberculosis (CNFy). CNF toxins deamidate and thereby constitutively activate RhoA, Rac1, and Cdc42. In this study, the effects of CNF1 on cell-matrix adhesion are analysed using functional cell-adhesion assays. CNF1 strongly increased cell-matrix binding of suspended Hela cells and decreased the susceptibly of cells to trypsin-induced cell detachment. Increased cell-matrix binding was also observed upon treatment of Hela cells with isomeric CNFy, that specifically deamidates RhoA. Increased cell-matrix binding thus appears to depend on RhoA deamidation. In contrast, increased cell spreading was specifically observed upon CNF1 treatment, suggesting that it rather depended on Rac1/Cdc42 deamidation. Increased cell-matrix adhesion is further presented to result in reduced cell migration of adherent cells. In contrast, migration of suspended cells was not affected upon treatment with CNF1 or CNFy. CNF1 and CNFy thus reduced cell migration specifically under the condition of pre-established cell-matrix adhesion.

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