Angiostatin Works as Immune Modulatory Molecules via Inhibition of Neutrophil Activation and Migration.
10.4167/jbv.2014.44.1.115
- Author:
So Youn WOO
1
Author Information
1. Department of Microbiology, School of Medicine, Ewha Womans University, Seoul, Korea. soyounwoo@ewha.ac.kr
- Publication Type:Letter
- Keywords:
Angiostatin;
Neutrophil;
Integrin alphavbeta3;
Lipid raft;
apoptosis
- MeSH:
Adenosine Triphosphate;
Angiostatins*;
Apoptosis;
Immunity, Innate;
Integrin alphaVbeta3;
Macrophages;
Neutrophil Activation*;
Neutrophils*;
Pathology;
Plasminogen;
Reactive Oxygen Species
- From:Journal of Bacteriology and Virology
2014;44(1):115-119
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Angiostatin is derived from enzymatic degradation of plasminogen and it has endogenous anti-angiogenic properties. Although tumor cells, macrophages, platelets, and neutrophils generate high amount of angiostatin, its expression is increased in inflammatory conditions. Moreover, angiostatin binds to integrin alpha(v)beta(3), ATP synthase, and angiomotin, which expressed on neutrophils. Activated neutrophils are essential to innate immune response, but also cause tissue damage through production of reactive oxygen species (ROS) and increase lifespan. In this article, it suggests several mechanism of angiostatin as immune regulator for neutrophils in inflammatory conditions; complex with integrin alpha(v)beta(3) and F(1)F(0) ATP synthase on lipid raft, attenuate polarization, and ROS production. These data provide possible exploit of double-edged role of neutrophils in acute inflammatory pathologies to preserve beneficial effect and minimize tissue damage.
