Integrin-Mediated Cell Adhesion and Spreading Engage Different Sources of Reactive Oxygen Species

2007 ◽  
Vol 9 (4) ◽  
pp. 469-481 ◽  
Author(s):  
Maria Letizia Taddei ◽  
Matteo Parri ◽  
Tommaso Mello ◽  
Alfonso Catalano ◽  
Alan D. Levine ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Adhesion ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Different Sources

scholarly journals CYP450 Mediates Reactive Oxygen Species Production in a Mouse Model of β-Thalassemia through an Increase in 20-HETE Activity

2021 ◽  
Vol 22 (3) ◽  
pp. 1106
Author(s):  
Rayan Bou-Fakhredin ◽  
Batoul Dia ◽  
Hilda E. Ghadieh ◽  
Stefano Rivella ◽  
Maria Domenica Cappellini ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mouse Model ◽  
Cell Injury ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Oxygen Species ◽  
Species Production ◽  
Different Sources ◽  
Dependent Pathway

Oxidative damage by reactive oxygen species (ROS) is one of the main contributors to cell injury and tissue damage in thalassemia patients. Recent studies suggest that ROS generation in non-transfusion-dependent (NTDT) patients occurs as a result of iron overload. Among the different sources of ROS, the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes and cytochrome P450 (CYP450) have been proposed to be major contributors for oxidative stress in several diseases. However, the sources of ROS in patients with NTDT remain poorly understood. In this study, Hbbth3/+ mice, a mouse model for β-thalassemia, were used. These mice exhibit an unchanged or decreased expression of the major NOX isoforms, NOX1, NOX2 and NOX4, when compared to their C57BL/6 control littermates. However, a significant increase in the protein synthesis of CYP4A and CYP4F was observed in the Hbbth3/+ mice when compared to the C57BL/6 control mice. These changes were paralleled by an increased production of 20-hydroxyeicosatetraenoic acid (20-HETE), a CYP4A and CYP4F metabolite. Furthermore, these changes corroborate with onset of ROS production concomitant with liver injury. To our knowledge, this is the first report indicating that CYP450 4A and 4F-induced 20-HETE production mediates reactive oxygen species overgeneration in Hbbth3/+ mice through an NADPH-dependent pathway.

Reactive oxygen species mediate Rac-induced loss of cell-cell adhesion in primary human endothelial cells

2002 ◽  
Vol 115 (9) ◽  
pp. 1837-1846 ◽  
Author(s):  
Sandra van Wetering ◽  
Jaap D. van Buul ◽  
Safira Quik ◽  
Frederik P. J. Mul ◽  
Eloise C. Anthony ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Cell Migration ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Reactive Oxygen ◽  
Small Gtpases ◽  
Endothelial Cell Migration ◽  
Oxygen Species ◽  
Cell Cell

The integrity of the endothelium is dependent on cell-cell adhesion, which is mediated by vascular-endothelial (VE)-cadherin. Proper VE-cadherin-mediated homotypic adhesion is, in turn, dependent on the connection between VE-cadherin and the cortical actin cytoskeleton. Rho-like small GTPases are key molecular switches that control cytoskeletal dynamics and cadherin function in epithelial as well as endothelial cells. We show here that a cell-penetrating, constitutively active form of Rac (Tat-RacV12) induces a rapid loss of VE-cadherin-mediated cell-cell adhesion in endothelial cells from primary human umbilical veins (pHUVEC). This effect is accompanied by the formation of actin stress fibers and is dependent on Rho activity. However,transduction of pHUVEC with Tat-RhoV14, which induces pronounced stress fiber and focal adhesion formation, did not result in a redistribution of VE-cadherin or an overall loss of cell-cell adhesion. In line with this observation, endothelial permeability was more efficiently increased by Tat-RacV12 than by Tat-RhoV14. The loss of cell-cell adhesion, which is induced by Tat-RacV12, occurred in parallel to and was dependent upon the intracellular production of reactive oxygen species (ROS). Moreover, Tat-RacV12 induced an increase in tyrosine phosphorylation of a component the VE-cadherin-catenin complex, which was identified as α-catenin. The functional relevance of this signaling pathway was further underscored by the observation that endothelial cell migration, which requires a transient reduction of cell-cell adhesion, was blocked when signaling through ROS was inhibited. In conclusion, Rac-mediated production of ROS represents a previously unrecognized means of regulating VE-cadherin function and may play an important role in the (patho)physiology associated with inflammation and endothelial damage as well as with endothelial cell migration and angiogenesis.

scholarly journals Reactive Oxygen Species as Essential Mediators of Cell Adhesion and Migration

2010 ◽  
Vol 98 (3) ◽  
pp. 576a ◽  
Author(s):  
Giuseppe Maulucci ◽  
Giovambattista Pani ◽  
Valentina Labate ◽  
Marina Mele ◽  
Emiliano Panieri ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Adhesion ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cell Adhesion And Migration ◽  
And Migration

scholarly journals Reactive oxygen species as essential mediators of cell adhesion

2003 ◽  
Vol 161 (5) ◽  
pp. 933-944 ◽  
Author(s):  
Paola Chiarugi ◽  
Giovambattista Pani ◽  
Elisa Giannoni ◽  
Letizia Taddei ◽  
Renata Colavitti ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Adhesion ◽  
Tyrosine Phosphatase ◽  
Adhesion Formation ◽  
Reactive Oxygen ◽  
Protein Tyrosine Phosphatases ◽  
Redox Signaling ◽  
Growth Factor Signaling ◽  
Oxygen Species ◽  
Protein Tyrosine

Signal transduction by reactive oxygen species (ROS; “redox signaling”) has recently come into focus in cellular biology studies. The signaling properties of ROS are largely due to the reversible oxidation of redox-sensitive target proteins, and especially of protein tyrosine phosphatases, whose activity is dependent on the redox state of a low pKa active site cysteine. A variety of mitogenic signals, including those released by receptor tyrosine kinase (RTKs) ligands and oncogenic H-Ras, involve as a critical downstream event the intracellular generation of ROS. Signaling by integrins is also essential for the growth of most cell types and is constantly integrated with growth factor signaling. We provide here evidence that intracellular ROS are generated after integrin engagement and that these oxidant intermediates are necessary for integrin signaling during fibroblast adhesion and spreading. Moreover, we propose a synergistic action of integrins and RTKs for redox signaling. Integrin-induced ROS are required to oxidize/inhibit the low molecular weight phosphotyrosine phosphatase, thereby preventing the enzyme from dephosphorylating and inactivating FAK. Accordingly, FAK phosphorylation and other downstream events, including MAPK phosphorylation, Src phosphorylation, focal adhesion formation, and cell spreading, are all significantly attenuated by inhibition of redox signaling. Hence, we have outlined a redox circuitry whereby, upon cell adhesion, oxidative inhibition of a protein tyrosine phosphatase promotes the phosphorylation/activation and the downstream signaling of FAK and, as a final event, cell adhesion and spreading onto fibronectin.

scholarly journals Impact of therapeutically induced reactive oxygen species and radical scavenging by α-tocopherol on tumor cell adhesion

2007 ◽  
Author(s):  
Oliver Thews ◽  
Christine Lambert ◽  
Debra Kelleher ◽  
Hans Biesalski ◽  
Peter Vaupel ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Adhesion ◽  
Tumor Cell ◽  
Radical Scavenging ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Cell Adhesion

scholarly journals Modification of oligosaccharides by reactive oxygen species decreases sialyl lewis x-mediated cell adhesion

Glycobiology ◽  
2005 ◽  
Vol 15 (11) ◽  
pp. 1094-1101 ◽  
Author(s):  
Hironobu Eguchi ◽  
Yoshitaka Ikeda ◽  
Tomomi Ookawara ◽  
Souichi Koyota ◽  
Noriko Fujiwara ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Adhesion ◽  
Reactive Oxygen ◽  
Sialyl Lewis X ◽  
Oxygen Species ◽  
Lewis X ◽  
Sialyl Lewis

scholarly journals Molecular Crosstalk between Integrins and Cadherins: Do Reactive Oxygen Species Set the Talk?

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Luca Goitre ◽  
Barbara Pergolizzi ◽  
Elisa Ferro ◽  
Lorenza Trabalzini ◽  
Saverio Francesco Retta
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Adhesion ◽  
Molecular Mechanisms ◽  
Immune Surveillance ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Functional Communication ◽  
Cellular Functions ◽  
Cell Matrix ◽  
Molecular Crosstalk

The coordinate modulation of the cellular functions of cadherins and integrins plays an essential role in fundamental physiological and pathological processes, including morphogenesis, tissue differentiation and renewal, wound healing, immune surveillance, inflammatory response, tumor progression, and metastasis. However, the molecular mechanisms underlying the fine-tuned functional communication between cadherins and integrins are still elusive. This paper focuses on recent findings towards the involvement of reactive oxygen species (ROS) in the regulation of cell adhesion and signal transduction functions of integrins and cadherins, pointing to ROS as emerging strong candidates for modulating the molecular crosstalk between cell-matrix and cell-cell adhesion receptors.

scholarly journals Common and Diverging Integrin Signals Downstream of Adhesion and Mechanical Stimuli and Their Interplay with Reactive Oxygen Species

2014 ◽  
Vol 09 (02) ◽  
pp. 159-171
Author(s):  
Kathrin Stephanie Zeller ◽  
Staffan Johansson
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Adhesion ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Integrin Signaling ◽  
Oxygen Species ◽  
Mechanical Stimuli ◽  
Basic Functions ◽  
Physical Forces ◽  
Integrin Family

The integrin family of adhesion receptors regulates basic functions of cells, and the signals they induce are altered in tumor cells. In this review we discuss how different integrin-dependent signals are generated during cell adhesion and by physical forces acting on cells. We also describe how reactive oxygen species are integral parts of integrin signaling and highlight a few important questions in the field. Answers to those may improve our understanding of integrins and their role in the development of cancer.

Sign in / Sign up

Export Citation Format

Share Document