دورية أكاديمية
أعرض في EDS

Mitochondrial calcium exchange links metabolism with the epigenome to control cellular differentiation.

التفاصيل البيبلوغرافية
العنوان: Mitochondrial calcium exchange links metabolism with the epigenome to control cellular differentiation.
المؤلفون: Lombardi AA; Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA., Gibb AA; Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA., Arif E; Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA., Kolmetzky DW; Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA., Tomar D; Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA., Luongo TS; Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA., Jadiya P; Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA., Murray EK; Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA., Lorkiewicz PK; Department of Medicine, Institute of Molecular Cardiology, Diabetes and Obesity Center, University of Louisville, Louisville, KY, 40202, USA., Hajnóczky G; Department of Pathology Anatomy and Cell Biology, MitoCare Center for Mitochondrial Imaging Research and Diagnostics, Thomas Jefferson University, Philadelphia, PA, 19107, USA., Murphy E; Systems Biology Center, National Heart Lung and Blood Institute, Bethesda, MD, 20892, USA., Arany ZP; Translational Research Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19014, USA., Kelly DP; Translational Research Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19014, USA., Margulies KB; Translational Research Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19014, USA., Hill BG; Department of Medicine, Institute of Molecular Cardiology, Diabetes and Obesity Center, University of Louisville, Louisville, KY, 40202, USA., Elrod JW; Center for Translational Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, 19140, USA. elrod@temple.edu.
المصدر: Nature communications [Nat Commun] 2019 Oct 04; Vol. 10 (1), pp. 4509. Date of Electronic Publication: 2019 Oct 04.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : Nature Pub. Group
مواضيع طبية MeSH: Calcium Signaling/*physiology , Cell Differentiation/*genetics , Epigenesis, Genetic/*physiology , Myocardial Infarction/*pathology , Myofibroblasts/*physiology, Animals ; Calcium Channels/genetics ; Calcium Channels/metabolism ; Calcium-Binding Proteins/metabolism ; DNA Methylation/physiology ; Disease Models, Animal ; Embryo, Mammalian ; Epigenome ; Female ; Fibrosis ; Glycolysis/physiology ; Humans ; Ketoglutaric Acids/metabolism ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Myocardial Infarction/diagnostic imaging ; Myocardial Infarction/etiology ; Myocardium/cytology ; Myocardium/pathology ; Primary Cell Culture
مستخلص: Fibroblast to myofibroblast differentiation is crucial for the initial healing response but excessive myofibroblast activation leads to pathological fibrosis. Therefore, it is imperative to understand the mechanisms underlying myofibroblast formation. Here we report that mitochondrial calcium ( m Ca 2+ ) signaling is a regulatory mechanism in myofibroblast differentiation and fibrosis. We demonstrate that fibrotic signaling alters gating of the mitochondrial calcium uniporter (mtCU) in a MICU1-dependent fashion to reduce m Ca 2+ uptake and induce coordinated changes in metabolism, i.e., increased glycolysis feeding anabolic pathways and glutaminolysis yielding increased α-ketoglutarate (αKG) bioavailability. m Ca 2+ -dependent metabolic reprogramming leads to the activation of αKG-dependent histone demethylases, enhancing chromatin accessibility in loci specific to the myofibroblast gene program, resulting in differentiation. Our results uncover an important role for the mtCU beyond metabolic regulation and cell death and demonstrate that m Ca 2+ signaling regulates the epigenome to influence cellular differentiation.
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معلومات مُعتمدة: R01 HL058493 United States HL NHLBI NIH HHS; P01 HL134608 United States HL NHLBI NIH HHS; R01 HL147844 United States HL NHLBI NIH HHS; R01 HL136954 United States HL NHLBI NIH HHS; R01 HL142271 United States HL NHLBI NIH HHS; R01 HL142864 United States HL NHLBI NIH HHS; R01 HL123966 United States HL NHLBI NIH HHS; R01 HL130174 United States HL NHLBI NIH HHS
المشرفين على المادة: 0 (Calcium Channels)
0 (Calcium-Binding Proteins)
0 (Ketoglutaric Acids)
0 (MICU1 protein, mouse)
0 (Mcu protein, mouse)
0 (Mitochondrial Membrane Transport Proteins)
0 (Mitochondrial Proteins)
تواريخ الأحداث: Date Created: 20191006 Date Completed: 20200214 Latest Revision: 20240421
رمز التحديث: 20240421
مُعرف محوري في PubMed: PMC6778142
DOI: 10.1038/s41467-019-12103-x
PMID: 31586055
قاعدة البيانات: MEDLINE
الوصف
تدمد:2041-1723
DOI:10.1038/s41467-019-12103-x