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Published on: May 12, 2023
Annexin 1 and neutrophil apoptosis
1The William Harvey Research Institute, Queen Mary University of London, Bart's and the London, Queen Mary School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK. M.Perretti@qmul.ac.uk
Abstract:
ANXA1 (annexin 1), a member of the 'annexin' family of calcium- and phospholipid-binding proteins, was originally identified as an endogenous mediator of the anti-inflammatory actions of glucocorticoids. However, this protein exerts multiple inhibitory effects on the host inflammatory response, including a preferential regulation of the adhesion step of blood-borne neutrophil within the microenvironment of an inflamed vasculature. It is now emerging that ANXA1 is endowed with other roles, since the protein is abundant in inflammatory exudates as it is produced and released by the extravasated neutrophil. In the present paper, we review the novel proapoptotic effect of ANXA1 and discuss its potential with respect to the pathophysiology of inflammation and leucocyte recruitment.
Insights
Annexin 1 (ANXA1), a protein regulating inflammation, also promotes apoptosis. This finding offers new insights into inflammation pathophysiology and leukocyte recruitment.
Area of Science:
- Biochemistry
- Immunology
- Cell Biology
Background:
- Annexin 1 (ANXA1) is known for mediating anti-inflammatory effects of glucocorticoids.
- ANXA1 regulates neutrophil adhesion in inflamed blood vessels.
- ANXA1 is found in inflammatory exudates and produced by neutrophils.
Purpose of the Study:
- To review the proapoptotic effects of ANXA1.
- To discuss the role of ANXA1 in inflammation and leukocyte recruitment.
Main Methods:
- Literature review of ANXA1 functions.
- Analysis of ANXA1's role in inflammatory processes.
Main Results:
- ANXA1 exhibits novel proapoptotic properties.
- ANXA1's functions extend beyond regulating neutrophil adhesion.
Conclusions:
- ANXA1's proapoptotic effect is significant for understanding inflammation.
- ANXA1 plays a complex role in the pathophysiology of inflammation and leukocyte recruitment.
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