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The Lipoxin Receptor ALX: Potent Ligand-Specific and Stereoselective Actions in Vivo

Nan Chiang, Charles N. Serhan, Sven-Erik Dahlén, Jeffrey M. Drazen, Douglas W. P. Hay, G. Enrico Rovati, Takao Shimizu, Takehiko Yokomizo and Charles Brink
Pharmacological Reviews September 2006, 58 (3) 463-487; DOI: https://doi.org/10.1124/pr.58.3.4
Nan Chiang
The Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine (N.C., C.N.S.), and Department of Medicine (J.M.D.), Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts; Department of Oral Medicine, Infection, and Immunity (C.N.S.), Harvard School of Dental Medicine, Boston, Massachusetts; Unit for Experimental Asthma and Allergy, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (S.-E.D.); GlaxoSmithKline, King of Prussia, Pennsylvania (D.W.P.H.); Division of Molecular Pharmacology, Pharmacological Sciences, Milan, Italy (G.E.R.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Tokyo, Tokyo, Japan (T.S.); Department of Medical Biochemistry, Graduate School of Medical Sciences, Kyushu University, Fu Kuoka, Japan (T.Y.); and Institut National de la Santé et de la Recherche Médicale U698, Hôpital Xavier Bichat secteur Claude Bernard, Paris, France (C.B.)
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Charles N. Serhan
The Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine (N.C., C.N.S.), and Department of Medicine (J.M.D.), Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts; Department of Oral Medicine, Infection, and Immunity (C.N.S.), Harvard School of Dental Medicine, Boston, Massachusetts; Unit for Experimental Asthma and Allergy, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (S.-E.D.); GlaxoSmithKline, King of Prussia, Pennsylvania (D.W.P.H.); Division of Molecular Pharmacology, Pharmacological Sciences, Milan, Italy (G.E.R.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Tokyo, Tokyo, Japan (T.S.); Department of Medical Biochemistry, Graduate School of Medical Sciences, Kyushu University, Fu Kuoka, Japan (T.Y.); and Institut National de la Santé et de la Recherche Médicale U698, Hôpital Xavier Bichat secteur Claude Bernard, Paris, France (C.B.)
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Sven-Erik Dahlén
The Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine (N.C., C.N.S.), and Department of Medicine (J.M.D.), Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts; Department of Oral Medicine, Infection, and Immunity (C.N.S.), Harvard School of Dental Medicine, Boston, Massachusetts; Unit for Experimental Asthma and Allergy, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (S.-E.D.); GlaxoSmithKline, King of Prussia, Pennsylvania (D.W.P.H.); Division of Molecular Pharmacology, Pharmacological Sciences, Milan, Italy (G.E.R.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Tokyo, Tokyo, Japan (T.S.); Department of Medical Biochemistry, Graduate School of Medical Sciences, Kyushu University, Fu Kuoka, Japan (T.Y.); and Institut National de la Santé et de la Recherche Médicale U698, Hôpital Xavier Bichat secteur Claude Bernard, Paris, France (C.B.)
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Jeffrey M. Drazen
The Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine (N.C., C.N.S.), and Department of Medicine (J.M.D.), Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts; Department of Oral Medicine, Infection, and Immunity (C.N.S.), Harvard School of Dental Medicine, Boston, Massachusetts; Unit for Experimental Asthma and Allergy, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (S.-E.D.); GlaxoSmithKline, King of Prussia, Pennsylvania (D.W.P.H.); Division of Molecular Pharmacology, Pharmacological Sciences, Milan, Italy (G.E.R.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Tokyo, Tokyo, Japan (T.S.); Department of Medical Biochemistry, Graduate School of Medical Sciences, Kyushu University, Fu Kuoka, Japan (T.Y.); and Institut National de la Santé et de la Recherche Médicale U698, Hôpital Xavier Bichat secteur Claude Bernard, Paris, France (C.B.)
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Douglas W. P. Hay
The Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine (N.C., C.N.S.), and Department of Medicine (J.M.D.), Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts; Department of Oral Medicine, Infection, and Immunity (C.N.S.), Harvard School of Dental Medicine, Boston, Massachusetts; Unit for Experimental Asthma and Allergy, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (S.-E.D.); GlaxoSmithKline, King of Prussia, Pennsylvania (D.W.P.H.); Division of Molecular Pharmacology, Pharmacological Sciences, Milan, Italy (G.E.R.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Tokyo, Tokyo, Japan (T.S.); Department of Medical Biochemistry, Graduate School of Medical Sciences, Kyushu University, Fu Kuoka, Japan (T.Y.); and Institut National de la Santé et de la Recherche Médicale U698, Hôpital Xavier Bichat secteur Claude Bernard, Paris, France (C.B.)
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G. Enrico Rovati
The Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine (N.C., C.N.S.), and Department of Medicine (J.M.D.), Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts; Department of Oral Medicine, Infection, and Immunity (C.N.S.), Harvard School of Dental Medicine, Boston, Massachusetts; Unit for Experimental Asthma and Allergy, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (S.-E.D.); GlaxoSmithKline, King of Prussia, Pennsylvania (D.W.P.H.); Division of Molecular Pharmacology, Pharmacological Sciences, Milan, Italy (G.E.R.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Tokyo, Tokyo, Japan (T.S.); Department of Medical Biochemistry, Graduate School of Medical Sciences, Kyushu University, Fu Kuoka, Japan (T.Y.); and Institut National de la Santé et de la Recherche Médicale U698, Hôpital Xavier Bichat secteur Claude Bernard, Paris, France (C.B.)
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Takao Shimizu
The Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine (N.C., C.N.S.), and Department of Medicine (J.M.D.), Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts; Department of Oral Medicine, Infection, and Immunity (C.N.S.), Harvard School of Dental Medicine, Boston, Massachusetts; Unit for Experimental Asthma and Allergy, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (S.-E.D.); GlaxoSmithKline, King of Prussia, Pennsylvania (D.W.P.H.); Division of Molecular Pharmacology, Pharmacological Sciences, Milan, Italy (G.E.R.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Tokyo, Tokyo, Japan (T.S.); Department of Medical Biochemistry, Graduate School of Medical Sciences, Kyushu University, Fu Kuoka, Japan (T.Y.); and Institut National de la Santé et de la Recherche Médicale U698, Hôpital Xavier Bichat secteur Claude Bernard, Paris, France (C.B.)
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Takehiko Yokomizo
The Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine (N.C., C.N.S.), and Department of Medicine (J.M.D.), Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts; Department of Oral Medicine, Infection, and Immunity (C.N.S.), Harvard School of Dental Medicine, Boston, Massachusetts; Unit for Experimental Asthma and Allergy, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (S.-E.D.); GlaxoSmithKline, King of Prussia, Pennsylvania (D.W.P.H.); Division of Molecular Pharmacology, Pharmacological Sciences, Milan, Italy (G.E.R.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Tokyo, Tokyo, Japan (T.S.); Department of Medical Biochemistry, Graduate School of Medical Sciences, Kyushu University, Fu Kuoka, Japan (T.Y.); and Institut National de la Santé et de la Recherche Médicale U698, Hôpital Xavier Bichat secteur Claude Bernard, Paris, France (C.B.)
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Charles Brink
The Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine (N.C., C.N.S.), and Department of Medicine (J.M.D.), Brigham and Women's Hospital/Harvard Medical School, Boston, Massachusetts; Department of Oral Medicine, Infection, and Immunity (C.N.S.), Harvard School of Dental Medicine, Boston, Massachusetts; Unit for Experimental Asthma and Allergy, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden (S.-E.D.); GlaxoSmithKline, King of Prussia, Pennsylvania (D.W.P.H.); Division of Molecular Pharmacology, Pharmacological Sciences, Milan, Italy (G.E.R.); Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Tokyo, Tokyo, Japan (T.S.); Department of Medical Biochemistry, Graduate School of Medical Sciences, Kyushu University, Fu Kuoka, Japan (T.Y.); and Institut National de la Santé et de la Recherche Médicale U698, Hôpital Xavier Bichat secteur Claude Bernard, Paris, France (C.B.)
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Abstract

Lipoxins (LXs) and aspirin-triggered LX (ATL) are trihydroxytetraene-containing eicosanoids generated from arachidonic acid that are distinct in structure, formation, and function from the many other proinflammatory lipid-derived mediators. These endogenous eicosanoids have now emerged as founding members of the first class of lipid/chemical mediators involved in the resolution of the inflammatory response. Lipoxin A4 (LXA4), ATL, and their metabolic stable analogs elicit cellular responses and regulate leukocyte trafficking in vivo by activating the specific receptor, ALX. ALX was the first receptor cloned and identified as a G protein-coupled receptor (GPCR) for lipoxygenase-derived eicosanoids with demonstrated cell type-specific signaling pathways. ALX at the level of DNA has sequence homology to the N-formylpeptide receptor and as an orphan GPCR was initially referred to as the N-formylpeptide receptor-like 1. Although LXA4 is the endogenous potent ligand for ALX activation, a number of peptides can also activate this receptor to stimulate calcium mobilization and chemotaxis in vitro. In contrast with LXA4, the counterparts of many of these peptides in vivo remain to be established. The purpose of this review is to highlight the molecular characterization of the ALX receptor and provide an overview of the ALX-LXA4 axis responsible for anti-inflammatory and proresolving signals in vivo. The information in this review provides further support for the initial nomenclature proposition for this GPCR as ALX.

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Pharmacological Reviews: 58 (3)
Pharmacological Reviews
Vol. 58, Issue 3
1 Sep 2006
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OtherReview Article

The Lipoxin Receptor ALX: Potent Ligand-Specific and Stereoselective Actions in Vivo

Nan Chiang, Charles N. Serhan, Sven-Erik Dahlén, Jeffrey M. Drazen, Douglas W. P. Hay, G. Enrico Rovati, Takao Shimizu, Takehiko Yokomizo and Charles Brink
Pharmacological Reviews September 1, 2006, 58 (3) 463-487; DOI: https://doi.org/10.1124/pr.58.3.4

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OtherReview Article

The Lipoxin Receptor ALX: Potent Ligand-Specific and Stereoselective Actions in Vivo

Nan Chiang, Charles N. Serhan, Sven-Erik Dahlén, Jeffrey M. Drazen, Douglas W. P. Hay, G. Enrico Rovati, Takao Shimizu, Takehiko Yokomizo and Charles Brink
Pharmacological Reviews September 1, 2006, 58 (3) 463-487; DOI: https://doi.org/10.1124/pr.58.3.4
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  • Article
    • Abstract
    • I. Introduction
    • II. Production of Lipoxins
    • III. Molecular Characterization of ALX, the Specific Receptor for Lipoxin A4
    • IV. Flexibility of G Protein-Coupled Ligand-Receptor Interaction: Lipid-versus Peptide-Derived Ligands
    • V. ALX: Historical Perspective and Connection to the FPR
    • VI. “Aspirin-Triggered” Lipoxin-Generating Systems
    • VII. Biological Significance of the Lipoxin-ALX System
    • VIII. How Does Lipoxin A4 Induce Anti-Inflammatory and Proresolving Signaling?
    • IX. Additional Receptors Involved in Lipoxin A4 and Aspirin-Triggered Lipoxin A4 in Vivo Actions
    • X. Conclusions
    • Acknowledgments
    • Footnotes
    • References
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