Prolyl Isomerase Pin1 Suppresses Thermogenic Programs in Adipocytes by Promoting Degradation of Transcriptional Co-activator PRDM16.

Adipocytes / cytology Animals DNA-Binding Proteins / genetics Mice Mice, Knockout NIMA-Interacting Peptidylprolyl Isomerase / genetics Protein Binding Proteolysis Thermogenesis / physiology Transcription Factors / genetics Transcription, Genetic / physiology Ubiquitination / physiology
PRDM16 Pin1 UCP-1 obesity thermogenesis

Journal

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

Informations de publication

Date de publication:
19 03 2019
Historique:
received: 27 07 2018
revised: 12 11 2018
accepted: 15 02 2019
entrez: 21 3 2019
pubmed: 21 3 2019
medline: 30 4 2020
Statut: ppublish

Résumé

Non-shivering thermogenesis in adipocytes provides defense against low temperatures and obesity development, but the underlying regulatory mechanism remains to be fully clarified. Based on both markedly increased Pin1 expression in states of excess nutrition and resistance to obesity development in Pin1 null mice, we speculated that adipocyte Pin1 may play a role in thermogenic programs. Adipose-specific Pin1 knockout (adPin1 KO) mice showed enhanced transcription of thermogenic genes and tolerance to hypothermia when exposed to cold. In addition, adPin1 KO mice were resistant to high-fat diet-induced obesity and glucose intolerance. A series of experiments revealed that Pin1 binds to PRDM16 and thereby promotes its degradation through the ubiquitin-proteasome system. Consistent with these results, Pin1 deletion in differentiated adipocytes showed enhancement of thermogenic programs in response to the β3 agonist CL316243 through the upregulation of PRDM16 proteins. These observations indicate that Pin1 is a negative regulator of non-shivering thermogenesis.

Identifiants

DOI: 10.1016/j.celrep.2019.02.066 PMID: 30893596
pubmed: 30893596
pii: S2211-1247(19)30245-1
doi: 10.1016/j.celrep.2019.02.066
pii:
doi:

Substances chimiques

DNA-Binding Proteins 0
NIMA-Interacting Peptidylprolyl Isomerase 0
Prdm16 protein, mouse 0
Transcription Factors 0
Pin1 protein, mouse EC 5.2.1.8

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

3221-3230.e3

Informations de copyright

Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.

Auteurs

Yusuke Nakatsu (Y)

Department of Medical Science, Graduate School of Medicine, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan.

Yasuka Matsunaga (Y)

Department of Medical Science, Graduate School of Medicine, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan.

Takeshi Yamamotoya (T)

Department of Medical Science, Graduate School of Medicine, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan.

Koji Ueda (K)

Department of Medical Science, Graduate School of Medicine, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan.

Masa-Ki Inoue (MK)

Department of Medical Science, Graduate School of Medicine, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan.

Yu Mizuno (Y)

Department of Medical Science, Graduate School of Medicine, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan.

Mikako Nakanishi (M)

Department of Medical Science, Graduate School of Medicine, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan.

Tomomi Sano (T)

Department of Periodontology, Division of Oral Rehabilitation, Faculty of Dental Science, Kyushu University, Fukuoka City, Fukuoka 812-8582, Japan.

Yosuke Yamawaki (Y)

Department of Cellular and Molecular Pharmacology, Division of Basic Life Sciences, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan.

Akifumi Kushiyama (A)

The Division of Diabetes and Metabolism, Institute for Adult Diseases, Asahi Life Foundation, Chuo-ku, Tokyo 103-0002, Japan.

Hideyuki Sakoda (H)

Department of Internal Medicine, The Division of Neurology, Respirology, Endocrinology, and Metabolism, Faculty of Medicine, University of Miyazaki, Kiyotake, Miyazaki 889-1692, Japan.

Midori Fujishiro (M)

The Division of Diabetes and Metabolic Diseases, Nihon University School of Medicine, Itabashi, Tokyo 173-8610, Japan.

Akihide Ryo (A)

The Department of Microbiology, Yokohama City University of Medicine, Yokohama City, Kanagawa 263-0004, Japan.

Hiraku Ono (H)

Department of Clinical Cell Biology, Chiba University Graduate School of Medicine, Chiba City, Chiba 260-8677, Japan.

Tohru Minamino (T)

Department of Cardiovascular Biology and Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata City, Niigata 951-8510, Japan.

Shin-Ichiro Takahashi (SI)

Department of Animal Sciences, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8567, Japan; Department of Applied Biological Chemistry, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8567, Japan.

Haruya Ohno (H)

Department of Molecular and Internal Medicine, Institute of Biomedical & Health Sciences, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan.

Masayasu Yoneda (M)

Department of Molecular and Internal Medicine, Institute of Biomedical & Health Sciences, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan.

Kei Takahashi (K)

Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, Miyagi 980-8575, Japan.

Hisamitsu Ishihara (H)

The Division of Diabetes and Metabolic Diseases, Nihon University School of Medicine, Itabashi, Tokyo 173-8610, Japan.

Hideki Katagiri (H)

Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, Miyagi 980-8575, Japan.

Fusanori Nishimura (F)

Department of Periodontology, Division of Oral Rehabilitation, Faculty of Dental Science, Kyushu University, Fukuoka City, Fukuoka 812-8582, Japan.

Takashi Kanematsu (T)

Department of Cellular and Molecular Pharmacology, Division of Basic Life Sciences, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan.

Tetsuya Yamada (T)

Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, Miyagi 980-8575, Japan; Department of Molecular Endocrinology and Metabolism, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113-8510, Japan.

Tomoichiro Asano (T)

Department of Medical Science, Graduate School of Medicine, Hiroshima University, Hiroshima City, Hiroshima 734-8553, Japan. Electronic address: tasano@hiroshima-u.ac.jp.

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Classifications MeSH

questionsmedicales.fr › Cellules › Cellules du tissu conjonctif › Adipocytes › Prolyl Isomerase Pin1 Suppresses Thermogenic...
questionsmedicales.fr › Eucaryotes › Animaux › Prolyl Isomerase Pin1 Suppresses Thermogenic...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines de liaison à l'ADN › Prolyl Isomerase Pin1 Suppresses Thermogenic...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Prolyl Isomerase Pin1 Suppresses Thermogenic...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Souris transgéniques › Souris knockout › Prolyl Isomerase Pin1 Suppresses Thermogenic...
questionsmedicales.fr › Enzymes et coenzymes › Enzymes › Isomerases › Cis-trans-isomerases › Peptidylpropyl isomerase › NIMA-interacting peptidylprolyl isomerase › Prolyl Isomerase Pin1 Suppresses Thermogenic...
questionsmedicales.fr › Métabolisme › Liaison aux protéines › Prolyl Isomerase Pin1 Suppresses Thermogenic...
questionsmedicales.fr › Métabolisme › Protéolyse › Prolyl Isomerase Pin1 Suppresses Thermogenic...
questionsmedicales.fr › Phénomènes biologiques › Adaptation biologique › Adaptation physiologique › Régulation de la température corporelle › Thermogenèse › Prolyl Isomerase Pin1 Suppresses Thermogenic...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Facteurs de transcription › Prolyl Isomerase Pin1 Suppresses Thermogenic...
questionsmedicales.fr › Phénomènes génétiques › Expression des gènes › Transcription génétique › Prolyl Isomerase Pin1 Suppresses Thermogenic...
questionsmedicales.fr › Phénomènes génétiques › Régulation de l'expression des gènes › Modification traductionnelle des protéines › Maturation post-traductionnelle des protéines › Ubiquitination › Prolyl Isomerase Pin1 Suppresses Thermogenic...