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Role of the protein C pathway in the extraintestinal thrombosis associated with murine colitis
Hideo Yoshida1, Janice Russell, Karen Y Stokes
1Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-33932, USA.
Gastroenterology
|June 3, 2008
Summary
Inflammatory bowel diseases (IBD) increase thrombosis risk. This study shows that the protein C pathway protects against extraintestinal thrombosis in dextran sodium sulfate (DSS)-induced colitis, highlighting its therapeutic potential.
Area of Science:
- Vascular Biology
- Inflammation and Immunology
- Thrombosis and Hemostasis
Background:
- Chronic inflammatory bowel diseases (IBD) are linked to a higher risk of thromboembolism, impacting patient morbidity and mortality.
- The precise mechanisms driving hypercoagulability in intestinal inflammation are not fully understood.
- Investigating the role of the protein C pathway in extraintestinal thrombosis associated with IBD is crucial.
Purpose of the Study:
- To investigate the contribution of the protein C pathway to enhanced extraintestinal thrombosis in dextran sodium sulfate (DSS)-induced colitis in mice.
- To determine if modulating the protein C pathway can mitigate thrombosis risk in a model of IBD.
Main Methods:
- Induction of microvascular thrombosis in cremaster muscle microvessels using a light/dye injury model in wild-type and colitic mice.
- Assessment of thrombosis formation in dextran sodium sulfate (DSS)-induced colitis models.
- Evaluation of thrombosis response in transgenic mice overexpressing the endothelial protein C receptor and in wild-type mice treated with activated protein C (APC) or an anti-APC antibody.
Main Results:
- Dextran sodium sulfate (DSS) colitis significantly enhanced thrombus formation in wild-type mice.
- Overexpression of the endothelial protein C receptor greatly attenuated the DSS-induced thrombosis response.
- Administration of activated protein C (APC) protected against thrombosis, while an anti-APC antibody exacerbated it.
Conclusions:
- Elevated levels of activated protein C (APC), whether endogenous or exogenous, provide protection against extraintestinal thrombosis associated with colonic inflammation.
- The protein C pathway plays a significant protective role in mitigating thrombosis risk during experimental colitis.
- Targeting the protein C pathway may offer a therapeutic strategy for managing thromboembolic complications in IBD.
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