scholarly journals Human mesenchymal stem cells express vascular cell phenotypes upon interaction with endothelial cell matrix

2009 ◽  
Vol 107 (4) ◽  
pp. 714-722 ◽  
Author(s):  
Thomas P. Lozito ◽  
Catherine K. Kuo ◽  
Juan M. Taboas ◽  
Rocky S. Tuan
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Endothelial Cell ◽  
Human Mesenchymal Stem Cells ◽  
Vascular Cell ◽  
Cell Matrix ◽  
Cell Phenotypes

scholarly journals IL-1β mediated nanoscale surface clustering of integrin α5β1 regulates the adhesion of mesenchymal stem cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Stephanie A. Maynard ◽  
Ekaterina Pchelintseva ◽  
Limor Zwi-Dantsis ◽  
Anika Nagelkerke ◽  
Sahana Gopal ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Spatial Organization ◽  
Human Mesenchymal Stem Cells ◽  
Super Resolution ◽  
Integrin Α5β1 ◽  
Cell Matrix ◽  
Cluster Area ◽  
Rapid Clearance ◽  
Resolution Imaging

AbstractClinical use of human mesenchymal stem cells (hMSCs) is limited due to their rapid clearance, reducing their therapeutic efficacy. The inflammatory cytokine IL-1β activates hMSCs and is known to enhance their engraftment. Consequently, understanding the molecular mechanism of this inflammation-triggered adhesion is of great clinical interest to improving hMSC retention at sites of tissue damage. Integrins are cell–matrix adhesion receptors, and clustering of integrins at the nanoscale underlies cell adhesion. Here, we found that IL-1β enhances adhesion of hMSCs via increased focal adhesion contacts in an α5β1 integrin-specific manner. Further, through quantitative super-resolution imaging we elucidated that IL-1β specifically increases nanoscale integrin α5β1 availability and clustering at the plasma membrane, whilst conserving cluster area. Taken together, these results demonstrate that hMSC adhesion via IL-1β stimulation is partly regulated through integrin α5β1 spatial organization at the cell surface. These results provide new insight into integrin clustering in inflammation and provide a rational basis for design of therapies directed at improving hMSC engraftment.

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