ArticleCell metabolism2015
Preserved DNA Damage Checkpoint Pathway Protects against Complications in Long-Standing Type 1 Diabetes.
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Article in Cell metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25citing papers in PubMed
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Who cites it
25 citing papers in PubMed.
- The role of DNA damage in diabetic complications.Nature reviews. Endocrinology · 2024Article
- Unraveling the Enigma of Organismal Death: Insights, Implications, and Unexplored Frontiers.Physiology (Bethesda, Md.) · 2024Review
- Protective Factors and the Pathogenesis of Complications in Diabetes.Endocrine reviews · 2024Review
- Genetics of diabetes.World journal of diabetes · 2023Review
- Far-red light-activated human islet-like designer cells enable sustained fine-tuned secretion of insulin for glucose control.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Signaling defects associated with insulin resistance in nondiabetic and diabetic individuals and modification by sex.The Journal of clinical investigation · 2021Article
- Discoveries from the study of longstanding type 1 diabetes.Diabetologia · 2021Review
- Diabetic Pneumopathy-A New Diabetes-Associated Complication: Mechanisms, Consequences and Treatment Considerations.Frontiers in endocrinology · 2021Review
- Leptin Receptor Signaling Regulates Protein Synthesis Pathways and Neuronal Differentiation in Pluripotent Stem Cells.Stem cell reports · 2020Article
- A Cell-Autonomous Signature of Dysregulated Protein Phosphorylation Underlies Muscle Insulin Resistance in Type 2 Diabetes.Cell metabolism · 2020Article
- The diabetic microenvironment causes mitochondrial oxidative stress in glomerular endothelial cells and pathological crosstalk with podocytes.Cell communication and signaling : CCS · 2020Article
- Compromised DNA repair is responsible for diabetes-associated fibrosis.The EMBO journal · 2020Article
- Article
- Insulin receptor-mediated signaling regulates pluripotency markers and lineage differentiation.Molecular metabolism · 2018Article
- The Vasoreparative Function of Myeloid Angiogenic Cells Is Impaired in Diabetes Through the Induction of IL1β.Stem cells (Dayton, Ohio) · 2018Article
- Circulating miRNA Profiles Associated With Hyperglycemia in Patients With Type 1 Diabetes.Diabetes · 2018Article
- High-glucose toxicity is mediated by AICAR-transformylase/IMP cyclohydrolase and mitigated by AMP-activated protein kinase inThe Journal of biological chemistry · 2018Article
- iPSC technology-based regenerative therapy for diabetes.Journal of diabetes investigation · 2018Review
- Diabetes Care Disparities in Long-standing Type 1 Diabetes in Canada and the U.S.: A Cross-sectional Comparison.Diabetes care · 2018Article
- Importance of long-term care of diabetic women starting in pregnancy.Diabetes/metabolism research and reviews · 2017Article
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Authors and funding
24 authors.
Shweta BhattSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA.
Manoj K GuptaSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA.
Mogher KhamaisiDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA; Section of Vascular Cell Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
Rachael MartinezSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
Marina A GritsenkoBiological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA.
Bridget K WagnerBroad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Patrick GuyeDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Volker BusskampDepartment of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Jun ShirakawaSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA.
Gongxiong WuSection of Vascular Cell Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
Chong Wee LiewSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA.
Therese R ClaussBiological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA.
Ivan ValdezSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA.
Abdelfattah El OuaamariSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA.
Ercument DiriceSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA.
Tomozumi TakataniSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA.
Hillary A KeenanDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA; Section of Vascular Cell Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
Richard D SmithBiological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA.
George ChurchDepartment of Genetics, Harvard Medical School, Boston, MA 02115, USA.
Ron WeissDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Amy J WagersSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA; Howard Hughes Medical Institute, Department of Stem Cell and Regenerative Biology, Harvard University, Harvard Stem Cell Institute, Cambridge, MA 02138, USA.
Wei-Jun QianBiological Sciences Division, Pacific Northwest National Laboratory, Richland, WA 99352, USA.
George L KingDepartment of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA; Section of Vascular Cell Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
Rohit N KulkarniSection of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA. Electronic address: rohit.kulkarni@joslin.harvard.edu.
Funding
SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI LAURIE J GOODYEAR · 1986 to 2026
$50.5MEquipment Supplement Request for a Research Resource for Ultra-sensitive High Throughput ProteomicsP41GM103493 · NIGMS · BATTELLE PACIFIC NORTHWEST LABORATORIES · PI SMITH, RICHARD D · 2012 to 2022
$22.6MRole of IGF-1 and Insulin Receptors Beta-Cell SurvivalR01DK067536 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 2004 to 2026
$8.0MValidation of Potential Protective Factors from Diabetic ComplicationsDP3DK094333 · NIDDK · JOSLIN DIABETES CENTER · PI KING, GEORGE L · 2011 to 2015
$4.1MRegulatory Networks and Biomarkers of Beta-cell Dysfunction and ApoptosisUC4DK104167 · NIDDK · BATTELLE PACIFIC NORTHWEST LABORATORIES · PI KULKARNI, ROHIT N., MATHEWS, CLAYTON E · 2014 to 2016
$2.7MRole of SerpinB1 in beta cell growthR01DK103215 · NIDDK · JOSLIN DIABETES CENTER · PI KULKARNI, ROHIT N. · 2014 to 2018
$2.6MGenetic circuits for high-throughput, multi-sensory, live cell microRNA profR01CA173712 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WEISS, RON · 2013 to 2017
$2.5MA Universal Multiplex Assay System for High-Throughput Clinical ApplicationsDP2OD006668 · OD · BATTELLE PACIFIC NORTHWEST LABORATORIES · PI QIAN, WEI-JUN · 2009 to 2009
$2.1MRole of the transcriptional coregulator, TRIP Br2, in adipocyte metabolismR00DK090210 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LIEW, CHONG WEE · 2012 to 2014
$724kRole of the transcriptional coregulator, TRIP Br2, in adipocyte metabolismK99DK090210 · NIDDK · JOSLIN DIABETES CENTER · PI LIEW, CHONG WEE · 2010 to 2011
$179kHoward Hughes Medical InstituteNCI NIH HHS R01 CA173712NIDDK NIH HHS DK036836NIDDK NIH HHS DP3 DK094333NIDDK NIH HHS DP3 DK094333-01NIDDK NIH HHS K99 DK090210NIDDK NIH HHS K99DK090210NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R00 DK090210NIDDK NIH HHS R00DK090210NIDDK NIH HHS R01 DK067536NIDDK NIH HHS R01 DK103215NIDDK NIH HHS R01 DK67536NIDDK NIH HHS UC4 DK104167NIDDK NIH HHS UC4 DK104167-01NIGMS NIH HHS P41 GM103493NIH HHS DP2 OD006668NIH HHS DP2OD006668PHS HHS R01 103215
Abstract
The mechanisms underlying the development of complications in type 1 diabetes (T1D) are poorly understood. Disease modeling of induced pluripotent stem cells (iPSCs) from patients with longstanding T1D (disease duration ≥ 50 years) with severe (Medalist +C) or absent to mild complications (Medalist -C) revealed impaired growth, reprogramming, and differentiation in Medalist +C. Genomics and proteomics analyses suggested differential regulation of DNA damage checkpoint proteins favoring protection from cellular apoptosis in Medalist -C. In silico analyses showed altered expression patterns of DNA damage checkpoint factors among the Medalist groups to be targets of miR200, whose expression was significantly elevated in Medalist +C serum. Notably, neurons differentiated from Medalist +C iPSCs exhibited enhanced susceptibility to genotoxic stress that worsened upon miR200 overexpression. Furthermore, knockdown of miR200 in Medalist +C fibroblasts and iPSCs rescued checkpoint protein expression and reduced DNA damage. We propose miR200-regulated DNA damage checkpoint pathway as a potential therapeutic target for treating complications of diabetes.
Indexed as
Cell Cycle CheckpointsDNA DamageGene Expression RegulationModels, BiologicalAgedDiabetes ComplicationsDiabetes Mellitus, Type 1FemaleHumansInduced Pluripotent Stem CellsMaleMicroRNAsMiddle AgedNeuronsMicroRNAsMIRN200 microRNA, human
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