Native adiponectin in serum binds to mammalian cells expressing T-cadherin, but not AdipoRs or calreticulin.


Journal

eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614

Informations de publication

Date de publication:
24 10 2019
Historique:
received: 22 05 2019
accepted: 13 10 2019
pubmed: 28 10 2019
medline: 12 3 2020
entrez: 25 10 2019
Statut: epublish

Résumé

Adiponectin is an adipocyte-derived atypically abundant circulating factor that protects various organs and tissues through its receptors, AdipoRs, calreticulin, and T-cadherin. To identify the major binding partner of circulating native adiponectin, we expressed these receptors on the surface of HEK293 cells. Adiponectin, either that in mouse or human serum, purified from serum, or produced by mammalian cells, bound to cells expressing T-cadherin, but not to those expressing AdipoR1 or calreticulin. The stable introduction of T-cadherin and AdipoR1 into CHO cells resulted in the cell surface localization of these receptors. Native adiponectin in serum bound to cells expressing T-cadherin, not to those expressing AdipoR1. The knockdown of T-cadherin, but not AdipoRs resulted in the significant attenuation of native adiponectin binding to C2C12 myotubes. Therefore, native adiponectin binding depended on the amount of T-cadherin expressed in HEK293 cells, CHO cells, and C2C12 myotubes. Collectively, our mammalian cell-based studies suggest that T-cadherin is the major binding partner of native adiponectin in serum.

Identifiants

pubmed: 31647413
doi: 10.7554/eLife.48675
pii: 48675
pmc: PMC6822988
doi:
pii:

Substances chimiques

Adiponectin 0
Cadherins 0
Calreticulin 0
H-cadherin 0
Receptors, Adiponectin 0

Banques de données

Dryad
['10.5061/dryad.82557c0']

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Japan Science and Technology Agency
ID : #16K09802
Pays : International
Organisme : Japan Science and Technology Agency
ID : #16K09801
Pays : International
Organisme : Japan Science and Technology Agency
ID : #15H04853
Pays : International
Organisme : Grant in Aid for Scientific Research
ID : #16K09802
Pays : International
Organisme : Grant in Aid for Scientific Research
ID : #16K09801
Pays : International
Organisme : Grant in Aid for Scientific Research
ID : #15H04853
Pays : International

Informations de copyright

© 2019, Kita et al.

Déclaration de conflit d'intérêts

SK, SF, NM, IS No competing interests declared

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Auteurs

Shunbun Kita (S)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Department of Adipose Management, Graduate School of Medicine, Osaka University, Osaka, Japan.

Shiro Fukuda (S)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.

Norikazu Maeda (N)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
Department of Metabolism and Atherosclerosis, Graduate School of Medicine, Osaka University, Osaka, Japan.

Iichiro Shimomura (I)

Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.

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Classifications MeSH