Myeloid ALX/FPR2 regulates vascularization following tissue injury.


Journal

Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876

Informations de publication

Date de publication:
23 06 2020
Historique:
pubmed: 10 6 2020
medline: 29 8 2020
entrez: 10 6 2020
Statut: ppublish

Résumé

Ischemic injury initiates a sterile inflammatory response that ultimately participates in the repair and recovery of tissue perfusion. Macrophages are required for perfusion recovery during ischemia, in part because they produce growth factors that aid in vascular remodeling. The input signals governing this pro-revascularization phenotype remain of interest. Here we found that hindlimb ischemia increases levels of resolvin D1 (RvD1), an inflammation-resolving lipid mediator that targets macrophages via its receptor, ALX/FPR2. Exogenous RvD1 enhances perfusion recovery during ischemia, and mice deficient in

Identifiants

pubmed: 32513697
pii: 1918163117
doi: 10.1073/pnas.1918163117
pmc: PMC7321964
doi:

Substances chimiques

FPR2 protein, human 0
Receptors, Formyl Peptide 0
Receptors, Lipoxin 0
formyl peptide receptor 2, mouse 0
resolvin D1 0
Docosahexaenoic Acids 25167-62-8

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

14354-14364

Subventions

Organisme : NIGMS NIH HHS
ID : P01 GM095467
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK124782
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL106173
Pays : United States

Déclaration de conflit d'intérêts

The authors declare no competing interest.

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Auteurs

Brian E Sansbury (BE)

Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115.

Xiaofeng Li (X)

Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115.

Blenda Wong (B)

Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115.

Andreas Patsalos (A)

Department of Medicine, Johns Hopkins University School of Medicine and Johns Hopkins All Children's Hospital, St. Petersburg, FL 33701.
Department of Biological Chemistry, Johns Hopkins University School of Medicine and Johns Hopkins All Children's Hospital, St. Petersburg, FL 33701.

Nikolas Giannakis (N)

Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.

Michael J Zhang (MJ)

Department of Medicine, University of Minnesota Medical School, Minneapolis, MN 55455.

Laszlo Nagy (L)

Department of Medicine, Johns Hopkins University School of Medicine and Johns Hopkins All Children's Hospital, St. Petersburg, FL 33701.
Department of Biological Chemistry, Johns Hopkins University School of Medicine and Johns Hopkins All Children's Hospital, St. Petersburg, FL 33701.
Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, H-4032 Debrecen, Hungary.

Matthew Spite (M)

Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115; mspite@bwh.harvard.edu.

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Classifications MeSH