Dkk3/REIC, an N-glycosylated Protein, Is a Physiological Endoplasmic Reticulum Stress Inducer in the Mouse Adrenal Gland.


Journal

Acta medica Okayama
ISSN: 0386-300X
Titre abrégé: Acta Med Okayama
Pays: Japan
ID NLM: 0417611

Informations de publication

Date de publication:
Jun 2020
Historique:
entrez: 25 6 2020
pubmed: 25 6 2020
medline: 2 4 2021
Statut: ppublish

Résumé

Dickkopf 3 (Dkk3) is a secreted protein belonging to the Dkk family and encoded by the orthologous gene of REIC. Dkk3/REIC is expressed by mouse and human adrenal glands, but the understanding of its roles in this organ is still limited. To determine the functions of Dkk3 in the mouse adrenal gland, we first identified that the mouse Dkk3 protein is N-glycosylated in the adrenal gland as well as in the brain. We performed proteome analysis on adrenal glands from Dkk3-null mice, in which exons 5 and 6 of the Dkk3 gene are deleted. Twodimensional polyacrylamide gel electrophoresis of adrenal proteins from wild-type and Dkk3-null mice revealed 5 protein spots whose intensities were altered between the 2 genotypes. Mass spectrometry analysis of these spots identified binding immunoglobulin protein (BiP), an endoplasmic reticulum (ER) chaperone. To determine whether mouse Dkk3 is involved in the unfolded protein response (UPR), we carried out a reporter assay using ER-stress responsive elements. Forced expression of Dkk3 resulted in the induction of distinct levels of reporter expression, showing the UPR initiated by the ER membrane proteins of activating transcription factor 6 (ATF6) and inositol-requring enzyme 1 (IRE1). Thus, it is possible that Dkk3 is a physiological ER stressor in the mouse adrenal gland.

Identifiants

pubmed: 32577017
doi: 10.18926/AMO/59950
doi:

Substances chimiques

Adaptor Proteins, Signal Transducing 0
DKK3 protein, human 0
Dkk3 protein, mouse 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

199-208

Déclaration de conflit d'intérêts

No potential conflict of interest relevant to this article was reported.

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Auteurs

Hirofumi Fujita (H)

Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.

Tetsuya Bando (T)

Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.

Seiichi Oyadomari (S)

Division of Molecular Biology, Institute for Genome Research, University of Tokushima, Tokushima 770-8503, Japan.

Kazuhiko Ochiai (K)

Department of Basic Science, School of Veterinary Nursing and Technology, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Musashino, Tokyo 180-8602, Japan.

Masami Watanabe (M)

Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.

Hiromi Kumon (H)

Innovation Center Okayama for Nanobio-Targeted Therapy, Okayama University, Okayama 700-8558, Japan.
Niimi University, Niimi, Okayama 718-8585, Japan.

Hideyo Ohuchi (H)

Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan.

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