Loss of function of transcription factor EB remodels lipid metabolism and cell death pathways in the cardiomyocyte.


Journal

Biochimica et biophysica acta. Molecular basis of disease
ISSN: 1879-260X
Titre abrégé: Biochim Biophys Acta Mol Basis Dis
Pays: Netherlands
ID NLM: 101731730

Informations de publication

Date de publication:
01 10 2020
Historique:
received: 18 12 2019
revised: 24 04 2020
accepted: 27 04 2020
pubmed: 22 5 2020
medline: 15 12 2020
entrez: 22 5 2020
Statut: ppublish

Résumé

Glucolipotoxicity following nutrient overload causes cardiomyocyte injury by inhibiting TFEB and suppressing lysosomal function. We ascertained whether in addition to the amount, the type of fatty acids (FAs) and duration of FA exposure regulate TFEB action and dictate cardiomyocyte viability. Saturated FA, palmitate, but not polyunsaturated FAs decreased TFEB content in a concentration- and time-dependent manner in cardiomyocytes. Hearts from high-fat high-sucrose diet-fed mice exhibited a temporal decline in nuclear TFEB content with marked elevation of diacylglycerol and triacylglycerol, suggesting that lipid deposition and TFEB loss are concomitant molecular events. Next, we examined the identity of signaling and metabolic pathways engaged by the loss of TFEB action in the cardiomyocyte. Transcriptome analysis in murine cardiomyocytes with targeted deletion of myocyte TFEB (TFEB

Identifiants

pubmed: 32437957
pii: S0925-4439(20)30177-0
doi: 10.1016/j.bbadis.2020.165832
pii:
doi:

Substances chimiques

Basic Helix-Loop-Helix Leucine Zipper Transcription Factors 0
Klf15 protein, mouse 0
Kruppel-Like Transcription Factors 0
Tcfeb protein, mouse 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

165832

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Purvi C Trivedi (PC)

Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, NS, Canada; Dalhousie Medicine New Brunswick, E2L 4L5 Saint John, NB, Canada.

Jordan J Bartlett (JJ)

Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, NS, Canada; Dalhousie Medicine New Brunswick, E2L 4L5 Saint John, NB, Canada.

Angella Mercer (A)

Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, NS, Canada; Dalhousie Medicine New Brunswick, E2L 4L5 Saint John, NB, Canada.

Logan Slade (L)

Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, NS, Canada; Dalhousie Medicine New Brunswick, E2L 4L5 Saint John, NB, Canada.

Marc Surette (M)

Department of Chemistry and Biochemistry, Université de Moncton, Moncton, NB, Canada.

Andrea Ballabio (A)

Telethon Institute of Genetics and Medicine, Via Pietro Castellino 111, 80131 Napoli, Italy.

Stephane Flibotte (S)

Department of Zoology, University of British Columbia, 4200 University Blvd, V6T 1Z4 Vancouver, BC, Canada.

Bahira Hussein (B)

Faculty of Pharmaceutical Sciences, University of British Columbia, 2405 Wesbrook Mall, V6T 1Z3 Vancouver, BC, Canada.

Brian Rodrigues (B)

Faculty of Pharmaceutical Sciences, University of British Columbia, 2405 Wesbrook Mall, V6T 1Z3 Vancouver, BC, Canada.

Petra C Kienesberger (PC)

Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, NS, Canada; Dalhousie Medicine New Brunswick, E2L 4L5 Saint John, NB, Canada.

Thomas Pulinilkunnil (T)

Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, NS, Canada; Dalhousie Medicine New Brunswick, E2L 4L5 Saint John, NB, Canada. Electronic address: tpulinil@dal.ca.

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Classifications MeSH