دورية أكاديمية

Metabolic Maturation Increases Susceptibility to Hypoxia-induced Damage in Human iPSC-derived Cardiomyocytes.

التفاصيل البيبلوغرافية
العنوان: Metabolic Maturation Increases Susceptibility to Hypoxia-induced Damage in Human iPSC-derived Cardiomyocytes.
المؤلفون: Peters MC; Department of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, Utrecht, The Netherlands., Maas RGC; Department of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, Utrecht, The Netherlands., van Adrichem I; Department of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, Utrecht, The Netherlands., Doevendans PAM; Department of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, Utrecht, The Netherlands., Mercola M; Cardiovascular Institute and Department of Medicine, Stanford University, Stanford, CA, USA., Šarić T; Center for Physiology and Pathophysiology, Institute for Neurophysiology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany., Buikema JW; Department of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, Utrecht, The Netherlands., van Mil A; Department of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, Utrecht, The Netherlands., Chamuleau SAJ; Department of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, Utrecht, The Netherlands.; Department of Cardiology, Amsterdam UMC Heart Center, Amsterdam, The Netherlands., Sluijter JPG; Department of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, Utrecht, The Netherlands., Hnatiuk AP; Cardiovascular Institute and Department of Medicine, Stanford University, Stanford, CA, USA., Neef K; Department of Cardiology, Laboratory of Experimental Cardiology, Regenerative Medicine Centre Utrecht, University Medical Centre Utrecht, University Utrecht, Utrecht, The Netherlands.
المصدر: Stem cells translational medicine [Stem Cells Transl Med] 2022 Oct 21; Vol. 11 (10), pp. 1040-1051.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Oxford University Press Country of Publication: England NLM ID: 101578022 Publication Model: Print Cited Medium: Internet ISSN: 2157-6580 (Electronic) Linking ISSN: 21576564 NLM ISO Abbreviation: Stem Cells Transl Med Subsets: MEDLINE
أسماء مطبوعة: Publication: 2022- : Oxford : Oxford University Press
Original Publication: Durham, NC : AlphaMed Press
مواضيع طبية MeSH: Induced Pluripotent Stem Cells* , Myocardial Ischemia*, Animals ; Humans ; Myocytes, Cardiac/metabolism ; Cell Differentiation ; Hypoxia/metabolism
مستخلص: The development of new cardioprotective approaches using in vivo models of ischemic heart disease remains challenging as differences in cardiac physiology, phenotype, and disease progression between humans and animals influence model validity and prognostic value. Furthermore, economical and ethical considerations have to be taken into account, especially when using large animal models with relevance for conducting preclinical studies. The development of human-induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) has opened new opportunities for in vitro studies on cardioprotective compounds. However, the immature cellular phenotype of iPSC-CMs remains a roadblock for disease modeling. Here, we show that metabolic maturation renders the susceptibility of iPSC-CMs to hypoxia further toward a clinically representative phenotype. iPSC-CMs cultured in a conventional medium did not show significant cell death after exposure to hypoxia. In contrast, metabolically matured (MM) iPSC-CMs showed inhibited mitochondrial respiration after exposure to hypoxia and increased cell death upon increased durations of hypoxia. Furthermore, we confirmed the applicability of MM iPSC-CMs for in vitro studies of hypoxic damage by validating the known cardioprotective effect of necroptosis inhibitor necrostatin-1. Our results provide important steps to improving and developing valid and predictive human in vitro models of ischemic heart disease.
(© The Author(s) 2022. Published by Oxford University Press.)
References: Artif Organs. 2017 May;41(5):452-460. (PMID: 27925238)
Cell Stem Cell. 2012 Jan 6;10(1):16-28. (PMID: 22226352)
Biochim Biophys Acta Mol Basis Dis. 2020 Oct 1;1866(10):165881. (PMID: 32562698)
Mol Med. 2018 Mar 15;24(1):3. (PMID: 30134787)
Cell Chem Biol. 2021 Mar 18;28(3):271-282. (PMID: 33740432)
Cell Stem Cell. 2020 Jun 4;26(6):862-879.e11. (PMID: 32459996)
Dev Cell. 2016 Dec 19;39(6):724-739. (PMID: 27997827)
Circulation. 2019 May 21;139(21):2451-2465. (PMID: 30866650)
Circulation. 2020 Mar 3;141(9):e139-e596. (PMID: 31992061)
Circulation. 2005 May 10;111(18):2276-9. (PMID: 15883223)
Cells. 2019 Sep 17;8(9):. (PMID: 31533262)
APL Bioeng. 2018 Mar 20;2(2):026102. (PMID: 31069299)
Cell Calcium. 2016 Mar;59(2-3):84-90. (PMID: 26922095)
Int J Cardiol. 2013 May 25;165(3):410-22. (PMID: 22459400)
Cardiovasc Res. 2013 Jul 1;99(1):83-91. (PMID: 23554461)
Pharmacol Ther. 2014 Mar;141(3):235-49. (PMID: 24140081)
Stem Cell Reports. 2018 Mar 13;10(3):834-847. (PMID: 29503093)
J Mol Cell Cardiol. 2014 Sep;74:340-52. (PMID: 24984146)
Basic Res Cardiol. 2012 Jul;107(4):270. (PMID: 22553001)
Cell Stem Cell. 2013 Jan 3;12(1):127-37. (PMID: 23168164)
Proc Natl Acad Sci U S A. 2018 Dec 26;115(52):E12245-E12254. (PMID: 30530645)
J Cardiovasc Pharmacol. 2010 Aug;56(2):130-40. (PMID: 20505524)
Cell Rep. 2020 Jul 21;32(3):107925. (PMID: 32697997)
Circ Res. 2018 Oct 12;123(9):1066-1079. (PMID: 30355156)
Pharmacol Rev. 2014 Oct;66(4):1142-74. (PMID: 25261534)
Cell Stem Cell. 2016 Sep 1;19(3):311-25. (PMID: 27545504)
Curr Mol Med. 2010 Oct;10(7):653-66. (PMID: 20712587)
Sci Rep. 2021 Feb 18;11(1):4153. (PMID: 33603154)
J Cell Mol Med. 2011 Jun;15(6):1239-53. (PMID: 21251211)
Sci Rep. 2016 Mar 15;6:23188. (PMID: 26976548)
Cardiovasc Res. 2018 Dec 1;114(14):1828-1842. (PMID: 30169602)
Physiol Rev. 1986 Jul;66(3):710-71. (PMID: 2942954)
Biochim Biophys Acta Mol Cell Res. 2020 Mar;1867(3):118471. (PMID: 30954570)
Stem Cells. 2013 May;31(5):829-37. (PMID: 23355363)
Semin Perinatol. 1996 Dec;20(6):542-63. (PMID: 9090780)
Circ Res. 2015 Jun 19;117(1):80-8. (PMID: 26089365)
Sci Rep. 2020 Oct 28;10(1):18498. (PMID: 33116175)
Genomics Proteomics Bioinformatics. 2016 Aug;14(4):207-15. (PMID: 27431744)
Stem Cells Transl Med. 2020 Oct;9(10):1121-1128. (PMID: 32725800)
Cell. 2007 Nov 30;131(5):861-72. (PMID: 18035408)
J Biol Chem. 2000 Feb 25;275(8):5997-6006. (PMID: 10681594)
Nat Methods. 2012 Jul;9(7):671-5. (PMID: 22930834)
Cardiovasc Res. 2020 Jun 1;116(7):1275-1287. (PMID: 31868875)
Cardiovasc Res. 2017 May 1;113(6):564-585. (PMID: 28453734)
Theranostics. 2019 Sep 25;9(24):7222-7238. (PMID: 31695764)
Am J Clin Nutr. 1991 Jan;53(1 Suppl):215S-222S. (PMID: 1845919)
معلومات مُعتمدة: R01 HL152055 United States HL NHLBI NIH HHS; 725229 International ERC_ European Research Council; 5P01HL141084 United States NH NIH HHS
فهرسة مساهمة: Keywords: cardiomyocytes; damage; hypoxia; induced pluripotent stem cells (iPSC); ischemia; metabolic maturation
تواريخ الأحداث: Date Created: 20220826 Date Completed: 20221025 Latest Revision: 20240125
رمز التحديث: 20240125
مُعرف محوري في PubMed: PMC9585948
DOI: 10.1093/stcltm/szac061
PMID: 36018047
قاعدة البيانات: MEDLINE
الوصف
تدمد:2157-6580
DOI:10.1093/stcltm/szac061