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A mitogenic action for fibrinogen mediated through intercellular adhesion molecule-1
1Joseph J. Jacobs Center for Thrombosis, and Vascular Biology/FF-2, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
The Journal of Biological Chemistry
|June 13, 1997
Summary
Fibrinogen binding to Intercellular adhesion molecule-1 (ICAM-1) stimulates cell proliferation. This effect, mediated by specific ICAM-1 and fibrinogen sequences, was blocked by anti-ICAM-1 antibodies.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Intercellular adhesion molecule-1 (ICAM-1) is crucial for leukocyte adhesion to the endothelium.
- ICAM-1 interacts with integrins and plasma protein fibrinogen.
Purpose of the Study:
- To investigate the effect of fibrinogen binding to ICAM-1 on cell proliferation.
- To identify the specific molecular interactions involved.
Main Methods:
- Assessing [3H]thymidine incorporation and direct cell counting in Raji cells and ICAM-1 transfected 293 cells.
- Utilizing anti-ICAM-1 monoclonal antibodies and purified ICAM-1 fragments.
- Testing fibrinogen fragments and synthetic peptides.
Main Results:
- Fibrinogen (200-800 nM) increased [3H]thymidine incorporation and cell counts in ICAM-1 expressing cells.
- This proliferative response was blocked by an anti-ICAM-1 antibody targeting the first Ig domain.
- Fibrinogen fragments and a specific fibrinogen gamma chain peptide also induced proliferation in ICAM-1 expressing cells.
Conclusions:
- Specific sequences within ICAM-1 and fibrinogen mediate a mitogenic signaling pathway.
- The interaction between ICAM-1 and fibrinogen promotes cellular proliferation.