The Map3k12 (Dlk)/JNK3 signaling pathway is required for pancreatic beta-cell proliferation during postnatal development.


Journal

Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402

Informations de publication

Date de publication:
Jan 2021
Historique:
received: 08 06 2019
accepted: 04 03 2020
pubmed: 20 3 2020
medline: 17 2 2021
entrez: 20 3 2020
Statut: ppublish

Résumé

Unveiling the key pathways underlying postnatal beta-cell proliferation can be instrumental to decipher the mechanisms of beta-cell mass plasticity to increased physiological demand of insulin during weight gain and pregnancy. Using transcriptome and global Serine Threonine Kinase activity (STK) analyses of islets from newborn (10 days old) and adult rats, we found that highly proliferative neonatal rat islet cells display a substantially elevated activity of the mitogen activated protein 3 kinase 12, also called dual leucine zipper-bearing kinase (Dlk). As a key upstream component of the c-Jun amino terminal kinase (Jnk) pathway, Dlk overexpression was associated with increased Jnk3 activity and was mainly localized in the beta-cell cytoplasm. We provide the evidence that Dlk associates with and activates Jnk3, and that this cascade stimulates the expression of Ccnd1 and Ccnd2, two essential cyclins controlling postnatal beta-cell replication. Silencing of Dlk or of Jnk3 in neonatal islet cells dramatically hampered primary beta-cell replication and the expression of the two cyclins. Moreover, the expression of Dlk, Jnk3, Ccnd1 and Ccnd2 was induced in high replicative islet beta cells from ob/ob mice during weight gain, and from pregnant female rats. In human islets from non-diabetic obese individuals, DLK expression was also cytoplasmic and the rise of the mRNA level was associated with an increase of JNK3, CCND1 and CCND2 mRNA levels, when compared to islets from lean and obese patients with diabetes. In conclusion, we find that activation of Jnk3 signalling by Dlk could be a key mechanism for adapting islet beta-cell mass during postnatal development and weight gain.

Identifiants

pubmed: 32189007
doi: 10.1007/s00018-020-03499-7
pii: 10.1007/s00018-020-03499-7
doi:

Substances chimiques

Ccnd1 protein, rat 0
Ccnd2 protein, rat 0
Cyclin D2 0
Insulin 0
RNA, Small Interfering 0
Cyclin D1 136601-57-5
Mitogen-Activated Protein Kinase 10 EC 2.7.1.-
MAP Kinase Kinase Kinases EC 2.7.11.25
mitogen-activated protein kinase kinase kinase 12 EC 2.7.11.25
Glucose IY9XDZ35W2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

287-298

Subventions

Organisme : Agence Nationale de la Recherche
ID : ANR-10-LABEX-46

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Auteurs

Mathie Tenenbaum (M)

Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, 59000, Lille, France. mathie.tenenbaum@univ-lille.fr.

Valérie Plaisance (V)

Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, 59000, Lille, France.
Univ. Lille, CNRS, Centrale Lille, ISEN, Univ. Valenciennes, UMR 8520, IEMN, 59000, Lille, France.

Raphael Boutry (R)

Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, 59000, Lille, France.

Valérie Pawlowski (V)

Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, 59000, Lille, France.
Univ. Lille, CNRS, Centrale Lille, ISEN, Univ. Valenciennes, UMR 8520, IEMN, 59000, Lille, France.

Cécile Jacovetti (C)

Department of Fundamental Neuroscience, University of Lausanne, Lausanne, Switzerland.

Clara Sanchez-Parra (C)

Department of Fundamental Neuroscience, University of Lausanne, Lausanne, Switzerland.

Hélène Ezanno (H)

Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, 59000, Lille, France.

Julien Bourry (J)

Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, 59000, Lille, France.

Nicole Beeler (N)

Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, 59000, Lille, France.

Gianni Pasquetti (G)

Univ. Lille, Inserm, CHU Lille, U1190-EGID, 59000, Lille, France.

Valery Gmyr (V)

Univ. Lille, Inserm, CHU Lille, U1190-EGID, 59000, Lille, France.

Stéphane Dalle (S)

Institut de Génomique Fonctionnelle, CNRS UMR5203, INSERM U1191, Montpellier University, Montpellier, France.

Julie Kerr-Conte (J)

Univ. Lille, Inserm, CHU Lille, U1190-EGID, 59000, Lille, France.

François Pattou (F)

Univ. Lille, Inserm, CHU Lille, U1190-EGID, 59000, Lille, France.

Syu-Ichi Hirai (SI)

Départment of Biology, Wakayama University, Wakayama, Japan.

Romano Regazzi (R)

Department of Fundamental Neuroscience, University of Lausanne, Lausanne, Switzerland.

Amélie Bonnefond (A)

Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, 59000, Lille, France.
Department of Medicine, Section of Genomics of Common Disease, Imperial College London, London, UK.

Philippe Froguel (P)

Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, 59000, Lille, France.
Department of Medicine, Section of Genomics of Common Disease, Imperial College London, London, UK.

Amar Abderrahmani (A)

Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8199-EGID, 59000, Lille, France. amar.abderrahmani@univ-lille.fr.
Univ. Lille, CNRS, Centrale Lille, ISEN, Univ. Valenciennes, UMR 8520, IEMN, 59000, Lille, France. amar.abderrahmani@univ-lille.fr.
Department of Medicine, Section of Genomics of Common Disease, Imperial College London, London, UK. amar.abderrahmani@univ-lille.fr.

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