Metallothionein 3 Controls the Phenotype and Metabolic Programming of Alternatively Activated Macrophages.


Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
25 06 2019
Historique:
received: 16 01 2019
revised: 01 05 2019
accepted: 22 05 2019
entrez: 27 6 2019
pubmed: 27 6 2019
medline: 31 7 2020
Statut: ppublish

Résumé

Alternatively activated (M2) macrophages promote wound healing but weaken antimicrobial defenses. The mechanisms that enforce macrophage divergence and dictate the phenotypic and metabolic characteristics of M2 macrophages remain elusive. We show that alternative activation with interleukin (IL)-4 induces expression of metallothionein 3 (MT3) that regulates macrophage polarization and function. MT3 was requisite for metabolic reprograming in IL-4-stimulated macrophages or M(IL-4) macrophages to promote mitochondrial respiration and suppress glycolysis. MT3 fostered an M(IL-4) phenotype, suppressed hypoxia inducible factor (HIF)1α activation, and thwarted the emergence of a proinflammatory M1 program in macrophages. MT3 deficiency augmented macrophage plasticity, resulting in enhanced interferon γ (IFNγ) responsiveness and a dampened M(IL-4) phenotype. Thus, MT3 programs the phenotype and metabolic fate of M(IL-4) macrophages.

Identifiants

pubmed: 31242420
pii: S2211-1247(19)30732-6
doi: 10.1016/j.celrep.2019.05.093
pmc: PMC6664296
mid: NIHMS1532877
pii:
doi:

Substances chimiques

Hif1a protein, mouse 0
Hypoxia-Inducible Factor 1, alpha Subunit 0
Il4 protein, mouse 0
Metallothionein 3 0
Mt3 protein, mouse 0
Nerve Tissue Proteins 0
Interleukin-4 207137-56-2

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

3873-3886.e7

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI133797
Pays : United States
Organisme : American Heart Association-American Stroke Association
ID : 19CDA34770022
Pays : United States
Organisme : American Heart Association-American Stroke Association
ID : 15POST25700182
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES006096
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI106269
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK099222
Pays : United States

Informations de copyright

Published by Elsevier Inc.

Auteurs

Debabrata Chowdhury (D)

Division of Infectious Diseases, College of Medicine, University of Cincinnati, Cincinnati, OH 45267, USA.

Hani Alrefai (H)

Division of Infectious Diseases, College of Medicine, University of Cincinnati, Cincinnati, OH 45267, USA; Department of Medical Biochemistry, Faculty of Medicine, Mansoura University, Mansoura 35516, Egypt.

Julio A Landero Figueroa (JA)

University of Cincinnati/Agilent Technologies Metallomics Center of the Americas, Department of Chemistry, University of Cincinnati, Cincinnati, OH 45221, USA.

Kathleen Candor (K)

University of Cincinnati/Agilent Technologies Metallomics Center of the Americas, Department of Chemistry, University of Cincinnati, Cincinnati, OH 45221, USA.

Aleksey Porollo (A)

Center for Autoimmune Genomics and Etiology and Division of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.

Roger Fecher (R)

Department of Pathology, Albert Einstein College of Medicine, Montefiore Medical Center, New York, NY 10467, USA.

Senad Divanovic (S)

Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45220, USA; Division of Immunobiology and Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.

George S Deepe (GS)

Division of Infectious Diseases, College of Medicine, University of Cincinnati, Cincinnati, OH 45267, USA.

Kavitha Subramanian Vignesh (K)

Division of Infectious Diseases, College of Medicine, University of Cincinnati, Cincinnati, OH 45267, USA. Electronic address: kavitha.subramanian@uc.edu.

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Classifications MeSH