دورية أكاديمية
أعرض في EDS

Endocardial/endothelial angiocrines regulate cardiomyocyte development and maturation and induce features of ventricular non-compaction.

التفاصيل البيبلوغرافية
العنوان: Endocardial/endothelial angiocrines regulate cardiomyocyte development and maturation and induce features of ventricular non-compaction.
المؤلفون: Rhee S; Department of Biology, Stanford University, Stanford, CA 94305, USA., Paik DT; Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford University, Stanford, CA, USA.; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA., Yang JY; Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford University, Stanford, CA, USA.; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA., Nagelberg D; Department of Biology, Stanford University, Stanford, CA 94305, USA., Williams I; Department of Biology, Stanford University, Stanford, CA 94305, USA.; Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA., Tian L; Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford University, Stanford, CA, USA.; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA., Roth R; Department of Biology, Stanford University, Stanford, CA 94305, USA., Chandy M; Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford University, Stanford, CA, USA.; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA., Ban J; Department of Biology, Stanford University, Stanford, CA 94305, USA., Belbachir N; Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford University, Stanford, CA, USA.; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA., Kim S; Department of Developmental Biology, Stanford University School of Medicine, Stanford University, Stanford, CA 94305, USA., Zhang H; Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford University, Stanford, CA, USA.; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA., Phansalkar R; Department of Genetics, Stanford University School of Medicine, Stanford University, Stanford, CA 94305, USA., Wong KM; Department of Biology, Stanford University, Stanford, CA 94305, USA., King DA; Department of Biology, Stanford University, Stanford, CA 94305, USA., Valdez C; Department of Biology, Stanford University, Stanford, CA 94305, USA., Winn VD; Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford University, Stanford, CA 94305, USA., Morrison AJ; Department of Biology, Stanford University, Stanford, CA 94305, USA., Wu JC; Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford University, Stanford, CA, USA.; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA., Red-Horse K; Department of Biology, Stanford University, Stanford, CA 94305, USA.; Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
المصدر: European heart journal [Eur Heart J] 2021 Nov 01; Vol. 42 (41), pp. 4264-4276.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
اللغة: English
بيانات الدورية: Publisher: Oxford University Press Country of Publication: England NLM ID: 8006263 Publication Model: Print Cited Medium: Internet ISSN: 1522-9645 (Electronic) Linking ISSN: 0195668X NLM ISO Abbreviation: Eur Heart J Subsets: MEDLINE
أسماء مطبوعة: Publication: 2005- : Oxford : Oxford University Press
Original Publication: London, Saunders [etc.]
مواضيع طبية MeSH: Endothelial Cells* , Myocytes, Cardiac*, Animals ; Endocardium ; Heart Ventricles ; Mice ; Myocardium
مستخلص: Aims: Non-compaction cardiomyopathy is a devastating genetic disease caused by insufficient consolidation of ventricular wall muscle that can result in inadequate cardiac performance. Despite being the third most common cardiomyopathy, the mechanisms underlying the disease, including the cell types involved, are poorly understood. We have previously shown that endothelial cell-specific deletion of the chromatin remodeller gene Ino80 results in defective coronary vessel development that leads to ventricular non-compaction in embryonic mouse hearts. We aimed to identify candidate angiocrines expressed by endocardial and endothelial cells (ECs) in wildtype and LVNC conditions in Tie2Cre;Ino80fl/fltransgenic embryonic mouse hearts, and test the effect of these candidates on cardiomyocyte proliferation and maturation.
Methods and Results: We used single-cell RNA-sequencing to characterize endothelial and endocardial defects in Ino80-deficient hearts. We observed a pathological endocardial cell population in the non-compacted hearts and identified multiple dysregulated angiocrine factors that dramatically affected cardiomyocyte behaviour. We identified Col15a1 as a coronary vessel-secreted angiocrine factor, downregulated by Ino80-deficiency, that functioned to promote cardiomyocyte proliferation. Furthermore, mutant endocardial and endothelial cells up-regulated expression of secreted factors, such as Tgfbi, Igfbp3, Isg15, and Adm, which decreased cardiomyocyte proliferation and increased maturation.
Conclusions: These findings support a model where coronary endothelial cells normally promote myocardial compaction through secreted factors, but that endocardial and endothelial cells can secrete factors that contribute to non-compaction under pathological conditions.
(Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.)
التعليقات: Comment in: Eur Heart J. 2021 Nov 1;42(41):4277-4279. doi: 10.1093/eurheartj/ehab304. (PMID: 34392349)
References: Hum Mol Genet. 2013 Dec 20;22(25):5107-20. (PMID: 23912340)
Nat Cell Biol. 2016 Oct;18(10):1031-42. (PMID: 27642787)
Dev Biol. 2000 Aug 15;224(2):263-74. (PMID: 10926765)
Development. 2009 Feb;136(3):495-505. (PMID: 19091769)
J Anat. 2017 Apr;230(4):575-588. (PMID: 28032348)
J Biol Chem. 2006 Mar 24;281(12):7816-24. (PMID: 16434404)
Circ Res. 2017 Sep 15;121(7):855-873. (PMID: 28912187)
Circ Res. 2010 Nov 12;107(10):1241-52. (PMID: 20847313)
Cell. 2009 Jul 23;138(2):257-70. (PMID: 19632177)
Neurology. 2010 Aug 24;75(8):732-41. (PMID: 20733148)
Development. 2013 May;140(9):1946-57. (PMID: 23571217)
Development. 2011 May;138(9):1795-805. (PMID: 21429986)
Oncogene. 2013 May 9;32(19):2412-20. (PMID: 22751133)
Eur Heart J. 2017 Dec 7;38(46):3449-3460. (PMID: 29029073)
Proc Natl Acad Sci U S A. 2005 Jul 19;102(29):10200-5. (PMID: 16009940)
Circ Arrhythm Electrophysiol. 2016 Apr;9(4):e003638. (PMID: 27069088)
Science. 2019 May 31;364(6443):865-870. (PMID: 31147515)
Nat Commun. 2018 Jan 25;9(1):368. (PMID: 29371594)
Cell Tissue Res. 1996 Dec;286(3):493-505. (PMID: 8929352)
Mech Dev. 2017 Apr;144(Pt A):92-101. (PMID: 27913119)
Peptides. 2001 Nov;22(11):1851-7. (PMID: 11754972)
J Biochem. 2006 Mar;139(3):391-8. (PMID: 16567404)
JCI Insight. 2019 Aug 22;4(16):. (PMID: 31434798)
J Signal Transduct. 2011;2011:521742. (PMID: 21637377)
Development. 2014 Dec;141(23):4500-12. (PMID: 25377552)
J Biol Chem. 2000 Oct 6;275(40):30907-15. (PMID: 10906123)
Nat Rev Cardiol. 2020 Aug;17(8):457-473. (PMID: 32231331)
Eur Heart J. 2018 Mar 7;39(10):864-873. (PMID: 29377983)
Integr Biol (Camb). 2013 Feb;5(2):390-401. (PMID: 23233209)
Pharmacol Rev. 2020 Jan;72(1):320-342. (PMID: 31871214)
Arthritis Res Ther. 2012 Apr 18;14(2):R80. (PMID: 22513098)
Biochem Biophys Res Commun. 2001 Sep 14;287(1):264-9. (PMID: 11549285)
J Biol Chem. 2002 Aug 2;277(31):28003-9. (PMID: 12034705)
Nat Rev Cardiol. 2017 Apr;14(4):224-237. (PMID: 28079110)
J Am Heart Assoc. 2019 Dec 3;8(23):e012993. (PMID: 31771441)
J Am Heart Assoc. 2014 Jul 28;3(4):. (PMID: 25085511)
JRSM Cardiovasc Dis. 2012 Aug 10;1(5):. (PMID: 24175071)
Nat Med. 2013 Feb;19(2):193-201. (PMID: 23314057)
J Biol Chem. 1992 Apr 15;267(11):7806-13. (PMID: 1373138)
Proc Natl Acad Sci U S A. 2001 Jan 30;98(3):1194-9. (PMID: 11158616)
J Am Coll Cardiol. 2018 Feb 20;71(7):711-722. (PMID: 29447731)
Nat Cell Biol. 2020 Jan;22(1):108-119. (PMID: 31915373)
Prog Growth Factor Res. 1995;6(2-4):215-22. (PMID: 8817664)
J Biol Chem. 2010 Feb 19;285(8):5258-65. (PMID: 20040604)
Development. 2017 Mar 15;144(6):1008-1017. (PMID: 28279973)
Nat Commun. 2015 Jan 19;6:6020. (PMID: 25597280)
Invest Ophthalmol Vis Sci. 2001 Apr;42(5):1080-6. (PMID: 11274089)
Development. 2015 Jan 1;142(1):21-30. (PMID: 25516967)
Circ Res. 2014 Jan 31;114(3):572-586. (PMID: 24481847)
Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15623-8. (PMID: 9861020)
Circ Res. 2018 Jan 5;122(1):74-87. (PMID: 29021295)
Cell. 2012 Nov 21;151(5):1083-96. (PMID: 23178125)
Nat Cell Biol. 2016 Jan;18(1):7-20. (PMID: 26641715)
Cell Cycle. 2019 Nov;18(21):2998-3009. (PMID: 31537150)
Cell Struct Funct. 2002 Feb;27(1):9-20. (PMID: 11937714)
معلومات مُعتمدة: R01 HL113006 United States HL NHLBI NIH HHS; R01 HL145676 United States HL NHLBI NIH HHS; R01 HL128503 United States HL NHLBI NIH HHS; F32 HL154514 United States HL NHLBI NIH HHS; R01 HL141371 United States HL NHLBI NIH HHS; R35 GM119580 United States GM NIGMS NIH HHS; R01 HL130020 United States HL NHLBI NIH HHS; P01 HL141084 United States HL NHLBI NIH HHS; T32 HL098049 United States HL NHLBI NIH HHS; K99 HL150216 United States HL NHLBI NIH HHS
فهرسة مساهمة: Keywords: Angiocrine factors; Cardiomyocyte maturation; Cardiomyocyte proliferation; Left ventricular non-compaction; Single-cell RNA-sequencing
تواريخ الأحداث: Date Created: 20210719 Date Completed: 20211108 Latest Revision: 20240923
رمز التحديث: 20240923
مُعرف محوري في PubMed: PMC8560211
DOI: 10.1093/eurheartj/ehab298
PMID: 34279605
قاعدة البيانات: MEDLINE
الوصف
تدمد:1522-9645
DOI:10.1093/eurheartj/ehab298