Platelet-derived growth factor signaling in pericytes promotes hypothalamic inflammation and obesity.

Inflammation Microglia Obesity Pericytes Platelet-derived growth factor

Journal

Molecular medicine (Cambridge, Mass.)
ISSN: 1528-3658
Titre abrégé: Mol Med
Pays: England
ID NLM: 9501023

Informations de publication

Date de publication:
05 Feb 2024
Historique:
received: 05 10 2023
accepted: 25 01 2024
medline: 6 2 2024
pubmed: 6 2 2024
entrez: 5 2 2024
Statut: epublish

Résumé

Pericytes are a vital component of the blood-brain barrier, and their involvement in acute inflammation was recently suggested. However, it remains unclear whether pericytes contribute to hypothalamic chronic inflammation and energy metabolism in obesity. The present study investigated the impact of pericytes on the pathophysiology of obesity by focusing on platelet-derived growth factor (PDGF) signaling, which regulates pericyte functions. Tamoxifen-inducible systemic conditional PDGF receptor β knockout mice (Pdgfrb Energy consumption increased and body weight gain decreased after high-fat diet loading in Pdgfrb PDGF receptor β signaling in hypothalamic pericytes promotes polarization of macrophages by changing their secretome and contributes to the progression of obesity.

Sections du résumé

BACKGROUND BACKGROUND
Pericytes are a vital component of the blood-brain barrier, and their involvement in acute inflammation was recently suggested. However, it remains unclear whether pericytes contribute to hypothalamic chronic inflammation and energy metabolism in obesity. The present study investigated the impact of pericytes on the pathophysiology of obesity by focusing on platelet-derived growth factor (PDGF) signaling, which regulates pericyte functions.
METHODS METHODS
Tamoxifen-inducible systemic conditional PDGF receptor β knockout mice (Pdgfrb
RESULTS RESULTS
Energy consumption increased and body weight gain decreased after high-fat diet loading in Pdgfrb
CONCLUSIONS CONCLUSIONS
PDGF receptor β signaling in hypothalamic pericytes promotes polarization of macrophages by changing their secretome and contributes to the progression of obesity.

Identifiants

pubmed: 38317079
doi: 10.1186/s10020-024-00793-z
pii: 10.1186/s10020-024-00793-z
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

21

Subventions

Organisme : JSPS KAKENHI
ID : JP21K08549
Organisme : JSPS KAKENHI
ID : 23H02957
Organisme : JST SPRING
ID : JPMJSP2145
Organisme : JST Moonshot R&D
ID : JPMJMS2021

Informations de copyright

© 2024. The Author(s).

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Auteurs

Akira Okekawa (A)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.

Tsutomu Wada (T)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan. twada@pha.u-toyama.ac.jp.

Yasuhiro Onogi (Y)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Research Center for Pre-Disease Science, University of Toyama, 2630 Sugitani, Toyama, Japan.

Yuki Takeda (Y)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.

Yuichiro Miyazawa (Y)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.

Masakiyo Sasahara (M)

Department of Pathology, University of Toyama, 2630 Sugitani, Toyama, Japan.

Hiroshi Tsuneki (H)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Department of Integrative Pharmacology, University of Toyama, 2630 Sugitani, Toyama, Japan.

Toshiyasu Sasaoka (T)

Department of Clinical Pharmacology, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan. tsasaoka@pha.u-toyama.ac.jp.

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