期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2010
卷号：107
期号：4
页码：1660-1665
DOI：10.1073/pnas.0907342107
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Endogenous mechanisms that act in the resolution of acute inflammation are essential for host defense and the return to homeostasis. Resolvin D1 (RvD1), biosynthesized during resolution, displays potent and stereoselective anti-inflammatory actions, such as limiting neutrophil infiltration and proresolving actions. Here, we demonstrate that RvD1 actions on human polymorphonuclear leukocytes (PMNs) are pertussis toxin sensitive, decrease actin polymerization, and block LTB4-regulated adhesion molecules ({beta}2 integrins). Synthetic [3H]-RvD1 was prepared, which revealed specific RvD1 recognition sites on human leukocytes. Screening systems to identify receptors for RvD1 gave two candidates--ALX, a lipoxin A4 receptor, and GPR32, an orphan--that were confirmed using a {beta}-arrestin-based ligand receptor system. Nuclear receptors including retinoid X receptor-{alpha} and peroxisome proliferator-activated receptor-{alpha
