-
Tytuł:
-
CD38 promotes angiotensin II-induced cardiac hypertrophy.
-
Autorzy:
-
Guan XH; Institute of Translational Medicine, Nanchang University, Nanchang, China.
Hong X; Institute of Translational Medicine, Nanchang University, Nanchang, China.
Zhao N; Institute of Translational Medicine, Nanchang University, Nanchang, China.
Liu XH; Institute of Translational Medicine, Nanchang University, Nanchang, China.
Xiao YF; Institute of Translational Medicine, Nanchang University, Nanchang, China.
Chen TT; Institute of Translational Medicine, Nanchang University, Nanchang, China.
Deng LB; Institute of Translational Medicine, Nanchang University, Nanchang, China.
Wang XL; Institute of Translational Medicine, Nanchang University, Nanchang, China.
Wang JB; Institute of Translational Medicine, Nanchang University, Nanchang, China.
Ji GJ; National Laboratory of Biomacromolecules, Institute of Biophysics Chinese Academy of Sciences, Beijing, China.
Fu M; Department of Basic Medical Science, Shock/Trauma Research Center, School of Medicine, University of Missouri Kansas City, Kansas City, MO, USA.
Deng KY; Institute of Translational Medicine, Nanchang University, Nanchang, China.
Xin HB; Institute of Translational Medicine, Nanchang University, Nanchang, China.
-
Źródło:
-
Journal of cellular and molecular medicine [J Cell Mol Med] 2017 Aug; Vol. 21 (8), pp. 1492-1502. Date of Electronic Publication: 2017 Mar 12.
-
Typ publikacji:
-
Journal Article
-
Język:
-
English
-
Imprint Name(s):
-
Publication: Oxford, England : Wiley-Blackwell
Original Publication: Bucharest : "Carol Davila" University Press, 2000-
-
MeSH Terms:
-
ADP-ribosyl Cyclase 1/*genetics
Angiotensin II/*pharmacology
Cardiomegaly/*genetics
Membrane Glycoproteins/*genetics
Myocardium/*metabolism
Myocytes, Cardiac/*metabolism
ADP-ribosyl Cyclase 1/antagonists & inhibitors ; ADP-ribosyl Cyclase 1/deficiency ; Animals ; Atrial Natriuretic Factor/genetics ; Atrial Natriuretic Factor/metabolism ; Calcium/metabolism ; Cardiomegaly/chemically induced ; Cardiomegaly/metabolism ; Cardiomegaly/pathology ; Cell Line ; Forkhead Box Protein O3/genetics ; Forkhead Box Protein O3/metabolism ; Gene Expression Regulation ; Membrane Glycoproteins/antagonists & inhibitors ; Membrane Glycoproteins/deficiency ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinase 1/genetics ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/genetics ; Mitogen-Activated Protein Kinase 3/metabolism ; Myocardium/pathology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/pathology ; NFATC Transcription Factors/genetics ; NFATC Transcription Factors/metabolism ; Natriuretic Peptide, Brain/genetics ; Natriuretic Peptide, Brain/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Rats ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Sirtuins/genetics ; Sirtuins/metabolism
-
References:
-
Antioxid Redox Signal. 2006 Nov-Dec;8(11-12):2111-24. (PMID: 17034354)
Stem Cells Int. 2016;2016:5720758. (PMID: 26798360)
J Biol Chem. 2010 Jan 29;285(5):3133-44. (PMID: 19940131)
Biochem Biophys Res Commun. 2010 Aug 20;399(2):167-72. (PMID: 20638362)
Annu Rev Immunol. 1997;15:707-47. (PMID: 9143705)
Curr Pharm Des. 2009;15(1):57-63. (PMID: 19149603)
Antioxid Redox Signal. 2012 Jun 15;16(12):1492-526. (PMID: 22229339)
Am J Physiol Heart Circ Physiol. 2006 Oct;291(4):H1545-53. (PMID: 16632544)
Cardiovasc Res. 2011 May 1;90(2):276-84. (PMID: 21115502)
J Biol Chem. 2009 Oct 23;284(43):29335-42. (PMID: 19696022)
J Biol Chem. 2002 Oct 4;277(40):37670-7. (PMID: 12163490)
Nat Med. 2012 Nov;18(11):1643-50. (PMID: 23086477)
Mol Cell Biochem. 2008 May;312(1-2):47-60. (PMID: 18292970)
N Engl J Med. 1990 May 31;322(22):1561-6. (PMID: 2139921)
J Mol Cell Cardiol. 2012 Nov;53(5):657-67. (PMID: 22921230)
Cell Metab. 2012 Jun 6;15(6):838-47. (PMID: 22682224)
J Biol Chem. 2005 Feb 11;280(6):4553-67. (PMID: 15574430)
J Biol Chem. 2005 May 27;280(21):20814-23. (PMID: 15781459)
FASEB J. 2002 May;16(7):697-705. (PMID: 11978734)
J Clin Invest. 2004 Oct;114(8):1058-71. (PMID: 15489953)
Proc Natl Acad Sci U S A. 1980 Mar;77(3):1588-92. (PMID: 6966400)
Cardiology. 2014;129(3):153-62. (PMID: 25277512)
Cell Metab. 2010 Dec 1;12(6):662-7. (PMID: 21109198)
Cardiovasc Res. 2004 Aug 15;63(3):467-75. (PMID: 15276472)
Am J Physiol Renal Physiol. 2005 Apr;288(4):F785-91. (PMID: 15598842)
Br J Pharmacol. 2013 Jan;168(1):117-28. (PMID: 22335191)
Cell. 1998 Apr 17;93(2):215-28. (PMID: 9568714)
Cardiovasc Drug Rev. 2007 Fall;25(3):235-60. (PMID: 17919258)
J Vasc Res. 2003 Jan-Feb;40(1):28-36. (PMID: 12644723)
J Clin Invest. 2009 Sep;119(9):2758-71. (PMID: 19652361)
Am J Physiol Heart Circ Physiol. 2015 Nov;309(9):H1375-89. (PMID: 26232232)
Nat Rev Mol Cell Biol. 2006 Aug;7(8):589-600. (PMID: 16936699)
Cold Spring Harb Symp Quant Biol. 2011;76:81-90. (PMID: 22114328)
Cardiovasc Res. 2010 Nov 1;88(2):250-6. (PMID: 20685942)
Physiol Genomics. 2011 Dec 16;43(24):1319-33. (PMID: 21954451)
Eur Heart J. 2008 May;29(10):1224-40. (PMID: 18424786)
Circ Res. 2010 Sep 3;107(5):659-66. (PMID: 20616315)
Science. 1993 Nov 12;262(5136):1056-9. (PMID: 8235624)
Genes Dev. 2006 Nov 1;20(21):2913-21. (PMID: 17079682)
Biochem Biophys Res Commun. 2006 Jul 14;345(4):1386-92. (PMID: 16730329)
Blood. 1998 Aug 15;92(4):1324-33. (PMID: 9694721)
J Cell Biol. 2000 Oct 2;151(1):117-30. (PMID: 11018058)
PLoS One. 2016 Mar 09;11(3):e0149125. (PMID: 26959359)
Biochem Biophys Res Commun. 2006 Oct 13;349(1):353-9. (PMID: 16935261)
Genomics. 2005 Feb;85(2):258-63. (PMID: 15676284)
Circulation. 2009 Apr 14;119(14 ):1941-9. (PMID: 19332462)
Circ Res. 2004 Jan 9;94(1):110-8. (PMID: 14656927)
Circ Res. 2008 Mar 28;102(6):703-10. (PMID: 18239138)
J Mol Cell Cardiol. 2002 Apr;34(4):379-88. (PMID: 11991728)
Toxicol Mech Methods. 2013 Jun;23(5):297-302. (PMID: 23256455)
J Immunol. 1990 Apr 1;144(7):2811-5. (PMID: 2319135)
Cardiovasc Res. 2007 Mar 1;73(4):667-77. (PMID: 17217938)
Mol Cell Biol. 2002 Apr;22(8):2799-809. (PMID: 11909972)
J Biol Chem. 2001 Feb 2;276(5):3524-30. (PMID: 11044444)
Oxid Med Cell Longev. 2016;2016:7410257. (PMID: 27547294)
-
Grant Information:
-
R15 AI138116 United States AI NIAID NIH HHS; R21 AI103618 United States AI NIAID NIH HHS
-
Contributed Indexing:
-
Keywords: CD38; NFATc4; SIRT3; angiotensin II; cardiac hypertrophy
-
Substance Nomenclature:
-
0 (FOXO3 protein, rat)
0 (Forkhead Box Protein O3)
0 (Membrane Glycoproteins)
0 (NFATC Transcription Factors)
0 (Nerve Tissue Proteins)
0 (Nfatc4 protein, rat)
0 (RNA, Small Interfering)
0 (Reactive Oxygen Species)
0 (SIRT3 protein, rat)
11128-99-7 (Angiotensin II)
114471-18-0 (Natriuretic Peptide, Brain)
85637-73-6 (Atrial Natriuretic Factor)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
EC 3.2.2.5 (Cd38 protein, mouse)
EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
EC 3.5.1.- (Sirtuins)
SY7Q814VUP (Calcium)
-
Entry Date(s):
-
Date Created: 20170316 Date Completed: 20180417 Latest Revision: 20201212
-
Update Code:
-
20240105
-
PubMed Central ID:
-
PMC5542907
-
DOI:
-
10.1111/jcmm.13076
-
PMID:
-
28296029
-
Cardiac hypertrophy is an early hallmark during the clinical course of heart failure and regulated by various signalling pathways. Recently, we observed that mouse embryonic fibroblasts from CD38 knockout mice were significantly resistant to oxidative stress such as H 2 O 2 -induced injury and hypoxia/reoxygenation-induced injury. In addition, we also found that CD38 knockout mice protected heart from ischaemia reperfusion injury through activating SIRT1/FOXOs-mediated antioxidative stress pathway. However, the role of CD38 in cardiac hypertrophy is not explored. Here, we investigated the roles and mechanisms of CD38 in angiotensin II (Ang-II)-induced cardiac hypertrophy. Following 14 days of Ang-II infusion with osmotic mini-pumps, a comparable hypertension was generated in both of CD38 knockout and wild-type mice. However, the cardiac hypertrophy and fibrosis were much more severe in wild-type mice compared with CD38 knockout mice. Consistently, RNAi-induced knockdown of CD38 decreased the gene expressions of atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) and reactive oxygen species generation in Ang-II-stimulated H9c2 cells. In addition, the expression of SIRT3 was elevated in CD38 knockdown H9c2 cells, in which SIRT3 may further activate the FOXO3 antioxidant pathway. The intracellular Ca 2+ release induced by Ang-II markedly decreased in CD38 knockdown H9c2 cells, which might be associated with the decrease of nuclear translocation of NFATc4 and inhibition of ERK/AKT phosphorylation. We concluded that CD38 plays an essential role in cardiac hypertrophy probably via inhibition of SIRT3 expression and activation of Ca 2+ -NFAT signalling pathway. Thus, CD38 may be a novel target for treating cardiac hypertrophy.
(© 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.)