Cell adhesion and matrix remodeling genes identified by co-expression analysis

2002 ◽  
Vol 3 (34) ◽  
pp. 109-112 ◽  
Author(s):  
Michael G. Walker ◽  
Wayne Volkmuth
Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1503 ◽  
Author(s):  
Hintermann ◽  
Christen

Fibrogenesis is a progressive scarring event resulting from disrupted regular wound healing due to repeated tissue injury and can end in organ failure, like in liver cirrhosis. The protagonists in this process, either liver-resident cells or patrolling leukocytes attracted to the site of tissue damage, interact with each other by soluble factors but also by direct cell–cell contact mediated by cell adhesion molecules. Since cell adhesion molecules also support binding to the extracellular matrix, they represent excellent biosensors, which allow cells to modulate their behavior based on changes in the surrounding microenvironment. In this review, we focus on selectins, cadherins, integrins and members of the immunoglobulin superfamily of adhesion molecules as well as some non-classical cell adhesion molecules in the context of hepatic fibrosis. We describe their liver-specific contributions to leukocyte recruitment, cell differentiation and survival, matrix remodeling or angiogenesis and touch on their suitability as targets in antifibrotic therapies.


PLoS ONE ◽  
2011 ◽  
Vol 6 (2) ◽  
pp. e14687 ◽  
Author(s):  
Andri K. Riau ◽  
Tina T. Wong ◽  
Sharon N. Finger ◽  
Shyam S. Chaurasia ◽  
Ai Hua Hou ◽  
...  

Author(s):  
Andri K. Riau ◽  
Tina T. Wong ◽  
Sharon N. Finger ◽  
Shyam S. Chaurasia ◽  
Ai Hua Hou ◽  
...  

2015 ◽  
Vol 309 (6) ◽  
pp. G475-G490 ◽  
Author(s):  
Cheryl de Vallière ◽  
Solange Vidal ◽  
Ieuan Clay ◽  
Giorgia Jurisic ◽  
Irina Tcymbarevich ◽  
...  

The pH-sensing receptor ovarian cancer G protein-coupled receptor 1 (OGR1; GPR68) is expressed in the gut. Inflammatory bowel disease is typically associated with a decrease in local pH, which may lead to altered epithelial barrier function and subsequent gastrointestinal repair involving epithelial cell adhesion and migration. As the mechanisms underlying the response to pH changes are not well understood, we have investigated OGR1-mediated, pH-dependent signaling pathways in intestinal epithelial cells. Caco-2 cells stably overexpressing OGR1 were created and validated as tools to study OGR1 signaling. Barrier function, migration, and proliferation were measured using electric cell-substrate impedance-sensing technology. Localization of the tight junction proteins zonula occludens protein 1 and occludin and the rearrangement of cytoskeletal actin were examined by confocal microscopy. Paracellular permeability and protein and gene expression analysis using DNA microarrays were performed on filter-grown Caco-2 monolayers. We report that an acidic pH shift from pH 7.8 to 6.6 improved barrier function and stimulated reorganization of filamentous actin with prominent basal stress fiber formation. Cell migration and proliferation during in vitro wound healing were inhibited. Gene expression analysis revealed significant upregulation of genes related to cytoskeleton remodeling, cell adhesion, and growth factor signaling. We conclude that acidic extracellular pH can have a signaling function and impact the physiology of intestinal epithelial cells. The deconstruction of OGR1-dependent signaling may aid our understanding of mucosal inflammation mechanisms.


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