scholarly journals Acheron, a Lupus antigen family member, regulates integrin expression, adhesion, and motility in differentiating myoblasts

2010 ◽  
Vol 298 (1) ◽  
pp. C46-C55 ◽  
Author(s):  
Honor L. Glenn ◽  
Zhaohui Wang ◽  
Lawrence M. Schwartz
Keyword(s):  
Growth Factors ◽  
Deletion Mutant ◽  
Laminin Receptor ◽  
Integrin Expression ◽  
Fibronectin Receptor ◽  
Substrate Adhesion ◽  
Matrix Interactions ◽  
And Migration ◽  
Extracellular Matrix Interactions

Acheron (Achn) was originally identified as novel gene that is induced when insect muscles become committed to die at the end of metamorphosis. In separate studies, we have demonstrated that Achn acts upstream of MyoD and is required by mammalian myoblasts to either differentiate or undergo apoptosis following loss of growth factors. In the present study we examined the role of Achn in regulating integrin-extracellular matrix interactions that are required for myogenesis. Both control C2C12 myoblasts and those engineered to express ectopic Achn expressed the fibronectin receptor integrin α5β1 in the presence of growth factors and the laminin receptor α7β1 following growth factor withdrawal. Expression of the laminin receptor was blocked in cells expressing either Achn antisense or an Achn deletion mutant that blocks differentiation. Control cells and those expressing ectopic Achn undergo sequential and transient increases in both substrate adhesion and migration before cell fusion. Blockade of Achn expression reduced these effects on laminin but not on fibronectin. Taken together, these data suggest that Achn may influence differentiation in part via its control of cell adhesion dynamics.

A potential role for the CDH13/CDH15 gene in repeat revascularization after first percutaneous coronary intervention

2020 ◽  
Vol 21 (2) ◽  
pp. 91-99
Author(s):  
Qian Xiang ◽  
Zhiyan Liu ◽  
Yun Lu ◽  
Jie Mao ◽  
Shuqing Chen ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Percutaneous Coronary Intervention ◽  
Potential Role ◽  
Coronary Intervention ◽  
Repeat Revascularization ◽  
Genetic Test Results ◽  
Percutaneous Coronary ◽  
Matrix Interactions ◽  
Extracellular Matrix Interactions

Aim: Major drawbacks of percutaneous coronary intervention are the high occurrence of repeat revascularization due to restenosis and disease progression. The aim of this study was to find genetic indicators to predict the risk of repeat revascularization. Materials & methods: From April 2015 to June 2016, 143 patients with percutaneous coronary intervention with genetic test results were enrolled. SNPs were measured by OmniZhongHua-8, and the SNPs in pathways genes related to known stenosis-related processes from the KEGG, BioCarta and Gene Cards databases were selected for analysis. Results: Cell–extracellular matrix interactions were the pathways with the most significant SNP ( CDH15 rs72819363) association with repeat revascularization. Compared with CDH13 rs11859453G carriers, the adjusted odds ratio for A carriers was 0.25 and 0.33 at 18 and 30 months. Conclusion: We demonstrated a potential role of the cell–extracellular matrix interactions pathway and the possible biomarker CDH13/CDH15 in the development of coronary repeat revascularization.

scholarly journals Insights into the local pathogenesis induced by fish toxins: Role of natterins and nattectin in the disruption of cell–cell and cell–extracellular matrix interactions and modulation of cell migration

Toxicon ◽  
2011 ◽  
Vol 58 (6-7) ◽  
pp. 509-517 ◽  
Author(s):  
Evilin Naname Komegae ◽  
Anderson Daniel Ramos ◽  
Ana Karina Oliveira ◽  
Solange Maria de Toledo Serrano ◽  
Mônica Lopes-Ferreira ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Migration ◽  
Matrix Interactions ◽  
Extracellular Matrix Interactions ◽  
Cell Cell

Depressed Immune Surveillance Against Cancer: Role of Deficient T Cell: Extracellular Matrix Interactions

1994 ◽  
Vol 2 (3) ◽  
pp. 225-233 ◽  
Author(s):  
A. Górski ◽  
V. Castronovo ◽  
B. Stepień-Sopniewska ◽  
P. Grieb ◽  
M. Ryba ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
T Cell ◽  
Immune Surveillance ◽  
Matrix Interactions ◽  
Extracellular Matrix Interactions

scholarly journals Role of integrin alpha 4 beta 7/alpha 4 beta P in lymphocyte adherence to fibronectin and VCAM-1 and in homotypic cell clustering

1992 ◽  
Vol 117 (1) ◽  
pp. 179-189 ◽  
Author(s):  
C Rüegg ◽  
AA Postigo ◽  
EE Sikorski ◽  
EC Butcher ◽  
R Pytela ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Surface Proteins ◽  
Fibronectin Receptor ◽  
Rgd Sequence ◽  
Cell Clustering ◽  
T Lymphoma Cells ◽  
Late Antigen ◽  
T Lymphoma ◽  
Extracellular Matrix Interactions

Integrins are heterodimeric cell surface proteins that mediate both cell-cell and cell-extracellular matrix interactions. We and others recently identified cDNAs encoding a novel integrin beta subunit, beta 7, in lymphocytes. We have now detected beta 7 mRNA in mouse TK-1 T lymphoma cells, which are known to express the putative Peyer's patch homing receptor alpha 4 beta P. We used an anti-peptide antiserum and a novel mAb against the beta 7 subunit to show that TK-1 cells express beta 7 as the only subunit associated with alpha 4. We conclude that beta 7 and beta P are identical. We also show that activated peripheral blood T cells express alpha 4 beta 7. We studied the function of alpha 4 beta 7/alpha 4 beta P in TK-1 cells, which do not express very late antigen (VLA)-4 (alpha 4 beta 1). Cells adhered to intact fibronectin and to a fibronectin fragment containing the CS-1 region, but not to a fragment containing the RGD sequence. Adhesion to fibronectin was inhibited by antibodies to alpha 4, suggesting that alpha 4 beta 7 is a fibronectin receptor. We confirmed that alpha 4 beta 7 binds to the CS-1 region of fibronectin using affinity chromatography. TK-1 cell adhesion to the vascular cell adhesion molecule VCAM-1 was also inhibited by antibodies to alpha 4, implying that alpha 4 beta 7 also plays a role in the adherence of lymphocytes to endothelial cells. TK-1 cell binding to fibronectin and VCAM-1 is markedly increased by brief PMA stimulation. We also found that mAbs against alpha 4 and beta 7 induce homotypic clustering of TK-1 cells. Taken together these results suggest that alpha 4 beta 7/alpha 4 beta P recognizes some or all of the same widely distributed ligands recognized by VLA-4 (alpha 4 beta 1) and that the role of alpha 4 beta 7/alpha 4 beta P may not be restricted to lymphocyte homing.

Platelet Contribution to Cancer Cell Growth and Migration: The Role of Platelet Growth Factors

1988 ◽  
Vol 18 (1) ◽  
pp. 18-28 ◽  
Author(s):  
Andreina Poggi ◽  
Elisa Vicenzi ◽  
Vittoria Cioce ◽  
Åke Wasteson
Keyword(s):  
Growth Factors ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cancer Cell Growth ◽  
Cell Growth And Migration ◽  
And Migration

scholarly journals Tissue architecture: the ultimate regulator of epithelial function?

1998 ◽  
Vol 353 (1370) ◽  
pp. 857-870 ◽  
Author(s):  
Carmen Hagios ◽  
André Lochter ◽  
Mina J. Bissell
Keyword(s):  
Cell Adhesion ◽  
Cell Shape ◽  
Tissue Structure ◽  
Tissue Architecture ◽  
Cell Behaviour ◽  
Matrix Interactions ◽  
Adhesive Interactions ◽  
And Function ◽  
Extracellular Matrix Interactions

The architecture of a tissue is defined by the nature and the integrity of its cellular and extracellular compartments, and is based on proper adhesive cell–cell and cell–extracellular matrix interactions. Cadherins and integrins are major adhesion–mediators that assemble epithelial cells together laterally and attach them basally to a subepithelial basement membrane, respectively. Because cell adhesion complexes are linked to the cytoskeleton and to the cellular signalling pathways, they represent checkpoints for regulation of cell shape and gene expression and thus are instructive for cell behaviour and function. This organization allows a reciprocal flow of mechanical and biochemical information between the cell and its microenvironment, and necessitates that cells actively maintain a state of homeostasis within a given tissue context. The loss of the ability of tumour cells to establish correct adhesive interactions with their microenvironment results in disruption of tissue architecture with often fatal consequences for the host organism. This review discusses the role of cell adhesion in the maintenance of tissue structure and analyses how tissue structure regulates epithelial function.

scholarly journals Role of Fibroblast Growth Factors Receptors (FGFRs) in Brain Tumors, Focus on Astrocytoma and Glioblastoma

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3825
Author(s):  
Alessio Ardizzone ◽  
Sarah A. Scuderi ◽  
Dario Giuffrida ◽  
Cristina Colarossi ◽  
Caterina Puglisi ◽  
...  
Keyword(s):  
Growth Factors ◽  
Brain Tumors ◽  
Fibroblast Growth Factors ◽  
Medical Emergency ◽  
Fibroblast Growth ◽  
Pharmacological Treatments ◽  
Biological Compounds ◽  
Depth Study ◽  
And Migration

Despite pharmacological treatments and surgical practice options, the mortality rate of astrocytomas and glioblastomas remains high, thus representing a medical emergency for which it is necessary to find new therapeutic strategies. Fibroblast growth factors (FGFs) act through their associated receptors (FGFRs), a family of tyrosine kinase receptors consisting of four members (FGFR1–4), regulators of tissue development and repair. In particular, FGFRs play an important role in cell proliferation, survival, and migration, as well as angiogenesis, thus their gene alteration is certainly related to the development of the most common diseases, including cancer. FGFRs are subjected to multiple somatic aberrations such as chromosomal amplification of FGFR1; mutations and multiple dysregulations of FGFR2; and mutations, translocations, and significant amplifications of FGFR3 and FGFR4 that correlate to oncogenesis process. Therefore, the in-depth study of these receptor systems could help to understand the etiology of both astrocytoma and glioblastoma so as to achieve notable advances in more effective target therapies. Furthermore, the discovery of FGFR inhibitors revealed how these biological compounds improve the neoplastic condition by demonstrating efficacy and safety. On this basis, this review focuses on the role and involvement of FGFRs in brain tumors such as astrocytoma and glioblastoma.

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