دورية أكاديمية
Deficiency of heme oxygenase 1a causes detrimental effects on cardiac function.
| العنوان: | Deficiency of heme oxygenase 1a causes detrimental effects on cardiac function. |
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| المؤلفون: | Wang H; Minerva Foundation Institute for Medical Research, Helsinki, Finland., Siren J; Minerva Foundation Institute for Medical Research, Helsinki, Finland., Perttunen S; Minerva Foundation Institute for Medical Research, Helsinki, Finland., Immonen K; Minerva Foundation Institute for Medical Research, Helsinki, Finland., Chen YC; Department of Anatomy, University of Helsinki, Helsinki, Finland., Narumanchi S; Minerva Foundation Institute for Medical Research, Helsinki, Finland., Kosonen R; Minerva Foundation Institute for Medical Research, Helsinki, Finland., Paavola J; Minerva Foundation Institute for Medical Research, Helsinki, Finland.; Heart and Lung Centre, University of Helsinki and Helsinki University Hospital, Helsinki, Finland., Laine M; Minerva Foundation Institute for Medical Research, Helsinki, Finland.; Heart and Lung Centre, University of Helsinki and Helsinki University Hospital, Helsinki, Finland., Tikkanen I; Minerva Foundation Institute for Medical Research, Helsinki, Finland.; Abdominal Centre Nephrology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland., Lakkisto P; Minerva Foundation Institute for Medical Research, Helsinki, Finland.; Department of Clinical Chemistry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland. |
| المصدر: | Journal of cellular and molecular medicine [J Cell Mol Med] 2024 Apr; Vol. 28 (7), pp. e18243. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Wiley-Blackwell Country of Publication: England NLM ID: 101083777 Publication Model: Print Cited Medium: Internet ISSN: 1582-4934 (Electronic) Linking ISSN: 15821838 NLM ISO Abbreviation: J Cell Mol Med Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Oxford, England : Wiley-Blackwell Original Publication: Bucharest : "Carol Davila" University Press, 2000- |
| مواضيع طبية MeSH: | Heme Oxygenase (Decyclizing)* , Cardiomyopathies*, Animals ; Humans ; Zebrafish/genetics ; Isoproterenol/pharmacology ; Heme Oxygenase-1/genetics ; Myocardium ; Hypoxia ; Myocytes, Cardiac |
| مستخلص: | Humans lacking heme oxygenase 1 (HMOX1) display growth retardation, haemolytic anaemia, and vulnerability to stress; however, cardiac function remains unclear. We aimed to explore the cardiac function of zebrafish lacking hmox1a at baseline and in response to stress. We generated zebrafish hmox1a mutants using CRISPR/Cas9 genome editing technology. Deletion of hmox1a increases cardiac output and further induces hypertrophy in adults. Adults lacking hmox1a develop myocardial interstitial fibrosis, restrain cardiomyocyte proliferation and downregulate renal haemoglobin and cardiac antioxidative genes. Larvae lacking hmox1a fail to respond to hypoxia, whereas adults are insensitive to isoproterenol stimulation in the heart, suggesting that hmox1a is necessary for cardiac response to stress. Haplodeficiency of hmox1a stimulates non-mitochondrial respiration and cardiac cell proliferation, increases cardiac output in larvae in response to hypoxia, and deteriorates cardiac function and structure in adults upon isoproterenol treatment. Intriguingly, haplodeficiency of hmox1a upregulates cardiac hmox1a and hmox1b in response to isoproterenol. Collectively, deletion of hmox1a results in cardiac remodelling and abrogates cardiac response to hypoxia and isoproterenol. Haplodeficiency of hmox1a aggravates cardiac response to the stress, which could be associated with the upregulation of hmox1a and hmox1b. Our data suggests that HMOX1 homeostasis is essential for maintaining cardiac function and promoting cardioprotective effects. (© 2024 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.) |
| References: | Gene. 2008 Feb 15;409(1-2):100-8. (PMID: 18178340) Front Cardiovasc Med. 2022 Aug 05;9:990013. (PMID: 35990947) EMBO Rep. 2020 Aug 5;21(8):e49752. (PMID: 32648304) Comp Biochem Physiol A Mol Integr Physiol. 2010 Aug;156(4):475-84. (PMID: 20363352) Eur J Pharmacol. 2018 Jan 5;818:57-66. (PMID: 29055786) Comp Biochem Physiol C Toxicol Pharmacol. 2017 Jan;191:138-151. (PMID: 27760386) Redox Biol. 2015 Dec;6:51-72. (PMID: 26184557) Nat Protoc. 2013 Apr;8(4):800-9. (PMID: 23538883) Cell Physiol Biochem. 2014;33(1):52-66. (PMID: 24401606) Int J Mol Cell Med. 2019 Fall;8(4):300-307. (PMID: 32587840) FASEB J. 1988 Jul;2(10):2557-68. (PMID: 3290025) Zebrafish. 2022 Feb;19(1):7-17. (PMID: 35108124) Stem Cell Res Ther. 2012 Dec 20;3(6):55. (PMID: 23257067) FASEB J. 2004 Apr;18(6):771-2. (PMID: 14977880) Diabetes. 2005 Mar;54(3):778-84. (PMID: 15734856) Circulation. 2010 May 4;121(17):1912-25. (PMID: 20404253) Transgenic Res. 2017 Feb;26(1):51-64. (PMID: 27778153) Hum Pathol. 2002 Jan;33(1):125-30. (PMID: 11823983) Can J Cardiol. 2016 Feb;32(2):160-8. (PMID: 26483091) J Clin Invest. 2007 Dec;117(12):3730-41. (PMID: 18037988) Cell Physiol Biochem. 2011;28(1):25-32. (PMID: 21865845) J Clin Invest. 1999 Jan;103(1):129-35. (PMID: 9884342) J Surg Res. 2009 Jul;155(1):147-56. (PMID: 19181338) Cardiovasc Res. 1998 Jan;37(1):91-100. (PMID: 9539862) Eur J Pharmacol. 2010 Jun 10;635(1-3):156-64. (PMID: 20303947) Toxicol Appl Pharmacol. 2016 Nov 15;311:74-87. (PMID: 27671773) J Cell Mol Med. 2024 Apr;28(7):e18243. (PMID: 38509740) Nat Protoc. 2016 Dec;11(12):2357-2375. (PMID: 27809318) Dis Model Mech. 2017 Jan 1;10(1):63-76. (PMID: 28067629) Blood. 2010 Dec 23;116(26):6054-62. (PMID: 20844238) Am J Physiol Heart Circ Physiol. 2000 Feb;278(2):H643-51. (PMID: 10666097) Int J Mol Sci. 2021 Feb 03;22(4):. (PMID: 33546372) J Pediatr Hematol Oncol. 2011 Jan;33(1):74-8. (PMID: 21088618) Am J Physiol Heart Circ Physiol. 2017 May 1;312(5):H1085-H1095. (PMID: 28341635) BMC Cancer. 2008 Jul 11;8:197. (PMID: 18620555) Biochem Pharmacol. 2011 Oct 1;82(7):769-77. (PMID: 21763292) Pediatr Rheumatol Online J. 2020 Oct 16;18(1):80. (PMID: 33066778) Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10919-24. (PMID: 9380735) Elife. 2019 Dec 23;8:. (PMID: 31868166) FEBS J. 2022 Feb;289(3):671-681. (PMID: 34544203) FEBS Lett. 2005 Oct 24;579(25):5494-500. (PMID: 16214137) J Exp Biol. 2016 May 15;219(Pt 10):1563-71. (PMID: 26994186) Int J Mol Sci. 2022 Sep 02;23(17):. (PMID: 36077457) Life Sci. 2020 Jul 15;253:117732. (PMID: 32360570) J Transl Med. 2014 Apr 05;12:89. (PMID: 24708733) Basic Res Cardiol. 2011 Nov;106(6):1367-77. (PMID: 21785893) Circ Res. 2022 Mar 4;130(5):741-759. (PMID: 35109669) Circ Res. 1958 Nov;6(6):765-70. (PMID: 13585605) Arch Biochem Biophys. 2021 Jan 15;697:108679. (PMID: 33248947) Circ Res. 2016 Jun 10;118(12):1940-1959. (PMID: 27283533) Int J Mol Sci. 2019 May 16;20(10):. (PMID: 31100876) PLoS One. 2019 May 23;14(5):e0217291. (PMID: 31120979) Blood. 2009 Jun 18;113(25):6449-60. (PMID: 19304954) Neuroscience. 2015 Dec 17;311:398-414. (PMID: 26523980) Eur J Pharmacol. 2011 Jun 1;659(2-3):199-205. (PMID: 21458444) |
| معلومات مُعتمدة: | Suomen Kulttuurirahasto; Sydäntutkimussäätiö; Finnish Foundation for Laboratory Medicine; Finska Läkaresällskapet; Aarne Koskelon Säätiö; Finnish state funding for university-level research; Ida Montinin Säätiö |
| فهرسة مساهمة: | Keywords: cardiac hypertrophy; cardiac output; heme oxygenase 1; interstitial fibrosis |
| المشرفين على المادة: | EC 1.14.14.18 (Heme Oxygenase (Decyclizing)) L628TT009W (Isoproterenol) EC 1.14.14.18 (Heme Oxygenase-1) |
| تواريخ الأحداث: | Date Created: 20240321 Date Completed: 20240322 Latest Revision: 20240716 |
| رمز التحديث: | 20240716 |
| مُعرف محوري في PubMed: | PMC10955162 |
| DOI: | 10.1111/jcmm.18243 |
| PMID: | 38509740 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1582-4934 |
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| DOI: | 10.1111/jcmm.18243 |