دورية أكاديمية
HDAC1: an environmental sensor regulating endothelial function.
| العنوان: | HDAC1: an environmental sensor regulating endothelial function. |
|---|---|
| المؤلفون: | Dunaway LS; Section of Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Kaul Genetics Building Room 802A, 720 20th Street South, Birmingham, AL 35233, USA., Pollock JS; Section of Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Kaul Genetics Building Room 802A, 720 20th Street South, Birmingham, AL 35233, USA. |
| المصدر: | Cardiovascular research [Cardiovasc Res] 2022 Jun 29; Vol. 118 (8), pp. 1885-1903. |
| نوع المنشور: | Journal Article; Review; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Oxford Journals Country of Publication: England NLM ID: 0077427 Publication Model: Print Cited Medium: Internet ISSN: 1755-3245 (Electronic) Linking ISSN: 00086363 NLM ISO Abbreviation: Cardiovasc Res Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2008- : Oxford : Oxford Journals Original Publication: London, British Medical Assn. |
| مواضيع طبية MeSH: | Histone Deacetylase 1*/metabolism , Nitric Oxide*/metabolism, Animals ; Antioxidants ; Endothelium ; Histone Deacetylases/metabolism ; Histones/metabolism |
| مستخلص: | The histone deacetylases (HDACs) are a family of enzymes that catalyse lysine deacetylation of both histone and non-histone proteins. Here, we review, summarize, and provide perspectives on the literature regarding one such HDAC, HDAC1, in endothelial biology. In the endothelium, HDAC1 mediates the effects of external and environmental stimuli by regulating major endothelial functions such as angiogenesis, inflammatory signalling, redox homeostasis, and nitric oxide signalling. Angiogenesis is most often, but not exclusively, repressed by endothelial HDAC1. The regulation of inflammatory signalling is more complex as HDAC1 promotes or suppresses inflammatory signalling depending upon the environmental stimuli. HDAC1 is protective in models of atherosclerosis where loss of HDAC1 results in increased cytokine and cell adhesion molecule (CAM) abundance. In other models, HDAC1 promotes inflammation by increasing CAMs and repressing claudin-5 expression. Consistently, from many investigations, HDAC1 decreases antioxidant enzyme expression and nitric oxide production in the endothelium. HDAC1 decreases antioxidant enzyme expression through the deacetylation of histones and transcription factors, and also regulates nitric oxide production through regulating both the expression and activity of nitric oxide synthase 3. The HDAC1-dependent regulation of endothelial function through the deacetylation of both histone and non-histone proteins ultimately impacts whole animal physiology and health. (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.) |
| References: | Biol Res. 2021 Mar 23;54(1):11. (PMID: 33757583) Circ Res. 2002 Nov 1;91(9):837-44. (PMID: 12411399) J Gerontol A Biol Sci Med Sci. 2019 May 16;74(6):787-793. (PMID: 30016403) EBioMedicine. 2020 Jan;51:102617. (PMID: 31911270) J Biol Chem. 2008 May 9;283(19):12686-90. (PMID: 18356165) Am J Physiol Heart Circ Physiol. 2014 Sep 1;307(5):H803-9. (PMID: 25015965) Eur J Clin Invest. 2003 Jul;33(7):536-42. (PMID: 12814388) Proc Natl Acad Sci U S A. 2020 Feb 11;117(6):3326-3336. (PMID: 31974313) FASEB J. 2019 Aug;33(8):9017-9029. (PMID: 31039328) PLoS One. 2014 Mar 21;9(3):e92793. (PMID: 24658119) Chonnam Med J. 2016 Jan;52(1):1-11. (PMID: 26865995) J Cell Biochem. 2010 Aug 15;110(6):1306-13. (PMID: 20564224) Mol Ther Nucleic Acids. 2020 Nov 05;23:577-591. (PMID: 33510945) J Neurosci. 2014 Sep 3;34(36):11929-47. (PMID: 25186741) J Biol Chem. 2005 Apr 22;280(16):16467-75. (PMID: 15722551) Nat Commun. 2016 Apr 25;7:11262. (PMID: 27109927) Cold Spring Harb Perspect Biol. 2014 Apr 01;6(4):a018713. (PMID: 24691964) J Clin Oncol. 2005 Jun 10;23(17):3912-22. (PMID: 15851766) Exp Diabetes Res. 2007;2007:21976. (PMID: 17641740) Clin Cancer Res. 2007 Sep 15;13(18 Pt 1):5411-7. (PMID: 17875771) J Biol Chem. 2005 Apr 22;280(16):16456-60. (PMID: 15716268) N Engl J Med. 1990 Jul 5;323(1):22-7. (PMID: 2355955) Eur J Pharmacol. 2018 Jan 5;818:371-380. (PMID: 29128366) Cell Death Differ. 2019 Oct;26(10):1970-1986. (PMID: 30670829) Oncogene. 2005 Mar 24;24(13):2204-17. (PMID: 15735762) J Biol Chem. 2015 Feb 13;290(7):4202-14. (PMID: 25512378) Blood. 2010 Jul 22;116(3):475-84. (PMID: 20203265) Cardiovasc Res. 2014 Mar 1;101(3):473-81. (PMID: 24323315) J Pharmacol Exp Ther. 2009 Nov;331(2):404-11. (PMID: 19692634) Science. 2009 Aug 14;325(5942):834-40. (PMID: 19608861) Arterioscler Thromb Vasc Biol. 2009 Mar;29(3):380-6. (PMID: 19122173) J Cell Mol Med. 2020 Jan;24(2):1713-1723. (PMID: 31782253) Biochem Soc Trans. 2013 Jun;41(3):741-9. (PMID: 23697933) J Biol Chem. 2019 Sep 20;294(38):13928-13938. (PMID: 31358618) Proc Natl Acad Sci U S A. 2012 Feb 7;109(6):1967-72. (PMID: 22308472) Front Pharmacol. 2020 May 27;11:629. (PMID: 32536862) Vascul Pharmacol. 2015 Aug;71:40-56. (PMID: 25869516) JCI Insight. 2020 Aug 20;5(16):. (PMID: 32673289) Hypertension. 2011 Mar;57(3):363-9. (PMID: 21263128) Oxid Med Cell Longev. 2017;2017:2143875. (PMID: 28392885) Mol Med Rep. 2018 Mar;17(3):4645-4650. (PMID: 29328474) J Biol Chem. 2012 Sep 14;287(38):32006-16. (PMID: 22822071) Adv Drug Deliv Rev. 2020;157:96-117. (PMID: 32579890) Diabetologia. 2021 Jan;64(1):226-239. (PMID: 33106900) Biochim Biophys Acta Gene Regul Mech. 2018 Oct;1861(10):962-970. (PMID: 30496041) Biochem Biophys Res Commun. 2006 Feb 3;340(1):29-34. (PMID: 16338217) Proc Natl Acad Sci U S A. 1995 May 9;92(10):4452-6. (PMID: 7538671) Sci Rep. 2016 Sep 27;6:34046. (PMID: 27669993) Nat Neurosci. 2017 Dec;20(12):1752-1760. (PMID: 29184215) Clin Cancer Res. 2008 Jul 15;14(14):4517-25. (PMID: 18579665) J Pharmacol Exp Ther. 2003 Nov;307(2):720-8. (PMID: 12975486) Int J Mol Sci. 2017 May 08;18(5):. (PMID: 28481295) J Biol Chem. 2005 Jul 1;280(26):24824-38. (PMID: 15870070) Nature. 2000 Nov 16;408(6810):377-81. (PMID: 11099047) Am J Respir Cell Mol Biol. 2015 Oct;53(4):513-24. (PMID: 25749103) Int J Mol Sci. 2020 Dec 18;21(24):. (PMID: 33353212) J Clin Biochem Nutr. 2017 Jul;61(1):6-13. (PMID: 28751803) Cytoskeleton (Hoboken). 2015 Oct;72(10):542-56. (PMID: 26403219) Circ Res. 2015 Jul 31;117(4):364-375. (PMID: 26123998) Mol Cell Biol. 2009 May;29(10):2658-72. (PMID: 19273602) Clin Exp Nephrol. 2012 Aug;16(4):518-21. (PMID: 22669535) J Biol Chem. 1995 Mar 10;270(10):5506-10. (PMID: 7890668) J Mol Cell Cardiol. 2018 Jan;114:309-319. (PMID: 29224834) J Biol Chem. 2003 Jul 4;278(27):24594-9. (PMID: 12716906) PLoS One. 2012;7(7):e42076. (PMID: 22848708) Can J Cardiol. 2017 Dec;33(12):1624-1632. (PMID: 29173602) Blood. 2007 Apr 1;109(7):2781-90. (PMID: 17179232) |
| معلومات مُعتمدة: | F31 HL149235 United States HL NHLBI NIH HHS; P01 HL136267 United States HL NHLBI NIH HHS; T32 DK116672 United States DK NIDDK NIH HHS |
| فهرسة مساهمة: | Keywords: Endothelium; Environmental sensor; HDAC1; Nitric oxide; Redox homeostasis |
| المشرفين على المادة: | 0 (Antioxidants) 0 (Histones) 31C4KY9ESH (Nitric Oxide) EC 3.5.1.98 (Histone Deacetylase 1) EC 3.5.1.98 (Histone Deacetylases) |
| تواريخ الأحداث: | Date Created: 20210715 Date Completed: 20220630 Latest Revision: 20231024 |
| رمز التحديث: | 20231215 |
| مُعرف محوري في PubMed: | PMC9239577 |
| DOI: | 10.1093/cvr/cvab198 |
| PMID: | 34264338 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1755-3245 |
|---|---|
| DOI: | 10.1093/cvr/cvab198 |