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S100A10 regulates plasminogen-dependent macrophage invasion
Paul A O'Connell1, Alexi P Surette, Robert S Liwski
1Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, Nova Scotia, Canada.
Blood
|April 29, 2010
Summary
The plasminogen receptor S100A10 is crucial for macrophage migration during inflammation. Mice lacking S100A10 show significantly reduced macrophage recruitment and invasion, highlighting its role in inflammatory responses.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- The plasminogen activation system is vital for macrophage migration.
- S100A10 is a known plasminogen receptor important in cancer cells.
- The role of S100A10 in macrophage migration is unexplored.
Purpose of the Study:
- To investigate the role of S100A10 in macrophage migration in response to inflammatory stimuli.
- To determine if S100A10 deficiency impacts macrophage recruitment and invasion.
Main Methods:
- Induction of peritoneal inflammation using thioglycollate in wild-type (WT) and S100A10-deficient (S100A10(-/-)) mice.
- Quantification of macrophage migration into the peritoneal cavity and Matrigel plugs.
- In vitro assessment of plasmin generation and invasion across a Matrigel barrier by WT and S100A10(-/-) macrophages.
Main Results:
- Macrophage migration into the peritoneal cavity was reduced by up to 53% in S100A10(-/-) mice.
- Infiltration of Matrigel plugs by S100A10(-/-) macrophages was reduced 8-fold compared to WT.
- S100A10(-/-) macrophages showed a 50% reduction in plasmin-dependent invasion and a 45% reduction in plasmin generation in vitro.
Conclusions:
- S100A10 plays a direct role in macrophage recruitment during inflammatory responses.
- S100A10 deficiency impairs macrophage migration and invasion, partly due to reduced plasmin and pro-MMP-9 activation.
- S100A10 is a key mediator of macrophage inflammatory response and migration.
