Oxytocin Suppresses Inflammatory Responses Induced by Lipopolysaccharide through Inhibition of the eIF-2-ATF4 Pathway in Mouse Microglia.


Journal

Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052

Informations de publication

Date de publication:
31 05 2019
Historique:
received: 13 05 2019
revised: 27 05 2019
accepted: 28 05 2019
entrez: 5 6 2019
pubmed: 5 6 2019
medline: 5 6 2019
Statut: epublish

Résumé

Microglia maintain brain homeostasis and modulate neuroinflammation and are implicated in the pathogenesis of various neurological diseases such as Alzheimer's disease. In this study, we found that in lipopolysaccharide (LPS)-stimulated microglia, the endoplasmic reticulum (ER) stress-related eIF-2-ATF4 pathway plays significant roles in TNF- and IL-6 production, as well as in the inflammasome-mediated production of IL-1. Furthermore, our analysis revealed that oxytocin (OT), a nonapeptide synthesized in the hypothalamus, suppressed the production of these proinflammatory cytokines by inhibiting activation of the eIF-2-ATF4 pathway. Our findings therefore suggest a novel anti-inflammatory axis of OT in activated microglia, which would be helpful for developing the novel effective strategies for regulating microglia-associated neuroinflammation.

Identifiants

pubmed: 31159306
pii: cells8060527
doi: 10.3390/cells8060527
pmc: PMC6627458
pii:
doi:

Substances chimiques

Atf4 protein, mouse 0
Cytokines 0
Eukaryotic Initiation Factor-2 0
Inflammasomes 0
Inflammation Mediators 0
Lipopolysaccharides 0
NF-kappa B 0
Activating Transcription Factor 4 145891-90-3
Oxytocin 50-56-6
p38 Mitogen-Activated Protein Kinases EC 2.7.11.24
Protein Tyrosine Phosphatase, Non-Receptor Type 1 EC 3.1.3.48
Ptpn1 protein, mouse EC 3.1.3.48

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Déclaration de conflit d'intérêts

The authors declare no conflict of interest.

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Auteurs

Takayuki Inoue (T)

Department of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan. taka2015.www@gmail.com.

Hajime Yamakage (H)

Department of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan. yamakage@satista.jp.

Masashi Tanaka (M)

Department of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan. masashi.7.tanaka@gmail.com.
Department of Physical Therapy, Health Science University, Yamanashi 401-0380, Japan. masashi.7.tanaka@gmail.com.

Toru Kusakabe (T)

Department of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan. kusakabe@kuhp.kyoto-u.ac.jp.

Akira Shimatsu (A)

Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan. ashimats@kyotolan.hosp.go.jp.

Noriko Satoh-Asahara (N)

Department of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan. nsatoh@kuhp.kyoto-u.ac.jp.

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Classifications MeSH