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Reduction of endoplasmic reticulummitochondria interactions in beta cells from patients with type 2 diabetes

PloS one, 2017-07 [Peer Reviewed Journal]

Distributed under a Creative Commons Attribution 4.0 International License ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0182027

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  • Title:
    Reduction of endoplasmic reticulummitochondria interactions in beta cells from patients with type 2 diabetes
  • Author: Thivolet, Charles ; Vial, Guillaume ; Cassel, Romeo ; Rieusset, Jennifer ; Madec, Anne- Marie
  • Subjects: Life Sciences
  • Is Part Of: PloS one, 2017-07
  • Description: Type 2 diabetes develops when beta cells are not able to fulfill insulin needs. The role of the endoplasmic reticulum±mitochondria junction in coordinating the functions of these two organelles throughout the natural history of type 2 diabetes is determinant and may explain the alterations of insulin biosynthesis. Our goal was to study endoplasmic reticulum and mitochondrial interactions in human beta cells from organ donors with type 2 diabetes. Pancreas samples were obtained via the network for pancreatic organ donors with diabetes (nPOD) based on disease status with 12 subjects with type 2 diabetes and 9 nondiabetic controls. We examined pancreatic specimens by immunofluorescence, in situ hybridization and in situ proximity ligation assay and compared the results to an in vitro model of beta-cell dysfunction. Expression of proteins that enable tethering andexchanges between endoplasmic reticulum (ER) and mitochondria and quantification of interconnection through mitochondria associated membranes (MAM) was investigated. In beta cells from type 2 diabetic cases as compared to controls, there was a significant increase in reticular expression of inositol triphosphate receptor-2 (IP3R2) both at the protein and mRNA levels, no difference in mitochondrial transit peptide receptor TOM20 and mitofusin-2 expressions, and a decrease in the expression of voltage-dependent anion channel-1 (VDAC-1). The number of IP3R2-VDAC-1 complexes identified by in situ proximity ligation assay was significantly lower in diabetic islets and in beta cells of diabetics ascompared to controls. Treatment of Min6-B1 cells with palmitate altered glucose-stimulated insulin secretion, increased ER stress and significantly reduced ER-mitochondrial interactions. We can conclude that specific changes in reticular and mitochondrial beta cell proteins characterize human type 2 diabetes with reduction in organelle interactions. This finding opens new targets of intervention.
  • Publisher: Public Library of Science
  • Language: English
  • Identifier: ISSN: 1932-6203
    EISSN: 1932-6203
    DOI: 10.1371/journal.pone.0182027
  • Source: Public Library of Science (PLoS) Journals Open Access
    Geneva Foundation Free Medical Journals at publisher websites
    Hyper Article en Ligne (HAL) (Open Access)
    ProQuest Databases
    PubMed Central
    DOAJ Directory of Open Access Journals
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