scholarly journals NADPH Oxidase 1 Controls the Persistence of Directed Cell Migration by a Rho-Dependent Switch of α2/α3 Integrins

2009 ◽  
Vol 29 (14) ◽  
pp. 3915-3928 ◽  
Author(s):  
Amine Sadok ◽  
Anne Pierres ◽  
Laetitia Dahan ◽  
Charles Prévôt ◽  
Maxime Lehmann ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Nadph Oxidase ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Directional Migration ◽  
Directed Cell Migration ◽  
Transient Activation ◽  
Nadph Oxidase 1 ◽  
Α3 Integrin

ABSTRACT NADPH oxidase 1 (Nox1) is expressed mainly in colon epithelial cells and produces superoxide ions as a primary function. We showed that Nox1 knockdown inhibits directional persistence of migration on collagen I. This paper dissects the mechanism by which Nox1 affects the direction of colonic epithelial cell migration in a two-dimensional model. Transient activation of Nox1 during cell spreading on collagen 1 temporarily inactivated RhoA and led to efficient exportation of α2β1 integrin to the cell surface, which supported persistent directed migration. Nox1 knockdown led to a loss of directional migration which takes place through a RhoA-dependent α2/α3 integrin switch. Transient RhoA overactivation upon Nox1 inhibition led to transient cytoskeletal reorganization and increased cell-matrix contact associated with a stable increase in α3 integrin cell surface expression. Blocking of α3 integrin completely reversed the loss of directional persistence of migration. In this model, Nox1 would represent a switch between random and directional migration through RhoA-dependent integrin cell surface expression modulation.

scholarly journals Endosomal Na+/H+ exchanger NHE5 influences MET recycling and cell migration

2016 ◽  
Vol 27 (4) ◽  
pp. 702-715 ◽  
Author(s):  
Steven Hung-Yi Fan ◽  
Yuka Numata ◽  
Masayuki Numata
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Tyrosine Kinases ◽  
Egf Receptor ◽  
Surface Expression ◽  
Mitogen Activated Protein Kinase ◽  
Cell Surface Expression ◽  
C6 Glioma Cells ◽  
Directed Cell Migration ◽  
Mitogen Activated Protein

Increased recycling and elevated cell surface expression of receptors serve as a mechanism for persistent receptor-mediated signaling. We show that the neuron-enriched Na+/H+ exchanger NHE5 is abundantly expressed in C6 glioma cells and plays an important part in regulating cell surface expression of the receptor tyrosine kinases MET and EGF receptor. NHE5 is associated with transferrin receptor (TfR)- and Rab11-positive recycling endosomal membranes, and NHE5 knockdown by short hairpin RNA significantly elevates pH of TfR-positive recycling endosomes. We present evidence that NHE5 facilitates MET recycling to the plasma membrane, protects MET from degradation, and modulates HGF-induced phosphatidylinositol-3-kinase and mitogen-activated protein kinase signaling. Moreover, NHE5 depletion abrogates Rac1 and Cdc42 signaling and actin cytoskeletal remodeling. We further show that NHE5 knockdown impairs directed cell migration and causes loss of cell polarity. Our study highlights a possible role of recycling endosomal pH in regulating receptor-mediated signaling through vesicular trafficking.

scholarly journals MIEN1, a novel interactor of Annexin A2, promotes tumor cell migration by enhancing AnxA2 cell surface expression

2015 ◽  
Vol 14 (1) ◽  
Author(s):  
Marilyne Kpetemey ◽  
Subhamoy Dasgupta ◽  
Smrithi Rajendiran ◽  
Susobhan Das ◽  
Lee D. Gibbs ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Tumor Cell ◽  
Surface Expression ◽  
Annexin A2 ◽  
Cell Surface Expression ◽  
Tumor Cell Migration

scholarly journals Engaged urokinase receptors enhance tumor breast cell migration and invasion by upregulating ?v?5 vitronectin receptor cell surface expression

2002 ◽  
Vol 102 (6) ◽  
pp. 562-571 ◽  
Author(s):  
Immacolata Silvestri ◽  
Immacolata Longanesi Cattani ◽  
Paola Franco ◽  
Giuseppe Pirozzi ◽  
Gerardo Botti ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Receptor Cell ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Migration And Invasion ◽  
Vitronectin Receptor ◽  
Cell Migration And Invasion

scholarly journals Matrix metalloproteinase-2 activation modulates glioma cell migration

1997 ◽  
Vol 110 (19) ◽  
pp. 2473-2482
Author(s):  
E.I. Deryugina ◽  
M.A. Bourdon ◽  
G.X. Luo ◽  
R.A. Reisfeld ◽  
A. Strongin
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Surface Expression ◽  
Matrix Proteins ◽  
Matrix Metalloproteinase 2 ◽  
Cell Surface Expression ◽  
Blocking Antibody ◽  
Tumor Cell Migration ◽  
Adhesion Sites ◽  
Glioma Cell Migration

Stable transfection of U251.3 glioma cells with cDNA encoding MT-MMP-1 resulted in increased cell surface expression of MT-MMP-1 and TIMP-2, constitutive activation of MMP-2 proenzyme and increased collagen degradation. In tumor spheroid outgrowth assays, cell migration of MT-MMP-1 transfectants relative to control was enhanced on collagen and decreased on vitronectin and fibronectin. These effects were reversed by TIMP-2 and were not associated with any substantial changes in cell adhesion. Binding of U251.3 cells to the C-terminal domain of MMP-2 was specifically inhibited by anti-(alpha)vss3 integrin blocking antibody indicating that MMP-2 interacts with (alpha)vss3 through the enzyme's C-terminal portion at or near the integrin's matrix adhesion sites. We propose that these mechanisms could govern directed matrix degradation in the tumor cells' microenvironment by sequestration of active MMP-2 on the cell surface. Our data suggest that activation of MMP-2 and its proteolytic activity localized to the cell surface could differentially modulate tumor cell migration in response to particular matrix proteins by altering both composition of the extracellular matrix and expression of adhesion receptors on the cell surface.

scholarly journals RAMP3 determines rapid recycling of atypical chemokine receptor-3 for guided angiogenesis

2019 ◽  
Vol 116 (48) ◽  
pp. 24093-24099 ◽  
Author(s):  
Duncan I. Mackie ◽  
Natalie R. Nielsen ◽  
Matthew Harris ◽  
Smriti Singh ◽  
Reema B. Davis ◽  
...  
Keyword(s):  
Cell Migration ◽  
G Protein ◽  
Chemokine Receptor ◽  
Chemokine Receptors ◽  
Resonance Energy Transfer ◽  
Resonance Energy ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Directed Cell Migration ◽  
Receptor Family

Receptor-activity–modifying proteins (RAMPs) are single transmembrane-spanning proteins which serve as molecular chaperones and allosteric modulators of G-protein–coupled receptors (GPCRs) and their signaling pathways. Although RAMPs have been previously studied in the context of their effects on Family B GPCRs, the coevolution of RAMPs with many GPCR families suggests an expanded repertoire of potential interactions. Using bioluminescence resonance energy transfer-based and cell-surface expression approaches, we comprehensively screen for RAMP interactions within the chemokine receptor family and identify robust interactions between RAMPs and nearly all chemokine receptors. Most notably, we identify robust RAMP interaction with atypical chemokine receptors (ACKRs), which function to establish chemotactic gradients for directed cell migration. Specifically, RAMP3 association with atypical chemokine receptor 3 (ACKR3) diminishes adrenomedullin (AM) ligand availability without changing G-protein coupling. Instead, RAMP3 is required for the rapid recycling of ACKR3 to the plasma membrane through Rab4-positive vesicles following either AM or SDF-1/CXCL12 binding, thereby enabling formation of dynamic spatiotemporal chemotactic gradients. Consequently, genetic deletion of either ACKR3 or RAMP3 in mice abolishes directed cell migration of retinal angiogenesis. Thus, RAMP association with chemokine receptor family members represents a molecular interaction to control receptor signaling and trafficking properties.

scholarly journals CXCR4 Mediates Enhanced Cell Migration in CALM-AF10 Leukemia

2022 ◽  
Vol 11 ◽  
Author(s):  
Shelby A. Fertal ◽  
Sayyed K. Zaidi ◽  
Janet L. Stein ◽  
Gary S. Stein ◽  
Jessica L. Heath
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Leukemia Cell ◽  
Chromosomal Translocation ◽  
Surface Expression ◽  
Receptor Expression ◽  
Cytokine Receptor ◽  
Cell Surface Expression ◽  
Tissue Cell ◽  
Valuable Insight

Leukemia transformed by the CALM-AF10 chromosomal translocation is characterized by a high incidence of extramedullary disease, central nervous system (CNS) relapse, and a poor prognosis. Invasion of the extramedullary compartment and CNS requires leukemia cell migration out of the marrow and adherence to the cells of the local tissue. Cell adhesion and migration are increasingly recognized as contributors to leukemia development and therapeutic response. These processes are mediated by a variety of cytokines, chemokines, and their receptors, forming networks of both secreted and cell surface factors. The cytokines and cytokine receptors that play key roles in CALM-AF10 driven leukemia are unknown. We find high cell surface expression of the cytokine receptor CXCR4 on leukemia cells expressing the CALM-AF10 oncogenic protein, contributing to the migratory nature of this leukemia. Our discovery of altered cytokine receptor expression and function provides valuable insight into the propagation and persistence of CALM-AF10 driven leukemia.

Persistent HIV Transcription Induces Sialyl-Lewis-X Glyco-Antigen Cell-Surface Expression

2020 ◽  
Author(s):  
Florent Colomb ◽  
Leila B. Giron ◽  
Leticia Kuri Cervantes ◽  
Tongcui Ma ◽  
Samson Adeniji ◽  
...  
Keyword(s):  
Cell Surface ◽  
Surface Expression ◽  
Sialyl Lewis X ◽  
Cell Surface Expression ◽  
Lewis X ◽  
Hiv Transcription ◽  
Sialyl Lewis

Influence of β-D-mannuronic acid, as a new member of non-steroidal anti-inflammatory drugs family, on expression pattern of chemokines and their receptors in rheumatoid arthritis

2019 ◽  
Vol 16 ◽  
Author(s):  
Mona Aslani ◽  
Arman Ahmadzadeh ◽  
Zahra Aghazadeh ◽  
Majid Zaki-Dizaji ◽  
Laleh Sharifi ◽  
...  
Keyword(s):  
Cell Surface ◽  
Mrna Expression ◽  
Surface Expression ◽  
Phase Iii ◽  
Cell Surface Expression ◽  
Optimum Dose ◽  
High Dose ◽  
Mannuronic Acid ◽  
Anti Inflammatory ◽  
High Doses

Background: : Based on the encouraging results of phase III clinical trial of β-D-mannuronic acid (M2000) (as a new anti-inflammatory drug) in patients with RA, in this study, we aimed to evaluate the effects of this drug on the expression of chemokines and their receptors in PBMCs of RA patients. Methods:: PBMCs of RA patients and healthy controls were separated and the patients' cells were treated with low, moderate and high doses (5, 25 and 50 μg/mL) of M2000 and optimum dose (1 μg/mL) of diclofenac, as a control in RPMI-1640 medium. Real-time PCR was used for evaluating the mRNA expression of CXCR3, CXCR4, CCR2, CCR5 and CCL2/MCP-1. Cell surface expression of CCR2 was investigated using flow cytometry. Results:: CCR5 mRNA expression reduced significantly, after treatment of the patients' cells with all three doses of M2000 and optimum dose of diclofenac. CXCR3 mRNA expression down-regulated significantly followed by treatment of these cells with moderate and high doses of M2000 and optimum dose of diclofenac. CXCR4 mRNA expression declined significantly after treatment of these cells with moderate and high doses of M2000. CCL2 mRNA expression significantly reduced only followed by treatment of these cells with high dose of M2000, whereas, mRNA and cell surface expressions of CCR2 diminished significantly followed by treatment of these cells with high dose of M2000 and optimum dose of diclofenac. Conclusion:: According to our results, M2000 through the down-regulation of chemokines and their receptors may restrict the infiltration of immune cells into the synovium.

Sign in / Sign up

Export Citation Format

Share Document