Hydrogen peroxide depolarizes mitochondria and inhibits IP <subscript>3</subscript> -evoked Ca <superscript>2+</superscript> release in the endothelium of intact arteries. - OpacWWW

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Tytuł:: Hydrogen peroxide depolarizes mitochondria and inhibits IP 3 -evoked Ca release in the endothelium of intact arteries.
Autorzy:: Zhang X; Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK.
Lee MD; Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK.
Wilson C; Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK.
McCarron JG; Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK. Electronic address: .
Źródło:: Cell calcium [Cell Calcium] 2019 Dec; Vol. 84, pp. 102108. Date of Electronic Publication: 2019 Nov 01.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: <2003->: Amsterdam : Elsevier
Original Publication: [Edinburgh, New York] Churchill Livingston
MeSH Terms:: Inositol 1,4,5-Trisphosphate Receptors*/metabolism
Endothelial Cells/*physiology
Hydrogen Peroxide/*metabolism
Mesenteric Arteries/*cytology
Mitochondria/*metabolism
Acetylcholine/metabolism ; Animals ; Calcium Signaling ; Carbonyl Cyanide m-Chlorophenyl Hydrazone/pharmacology ; Cells, Cultured ; Feedback, Physiological ; Inositol 1,4,5-Trisphosphate/metabolism ; Membrane Potential, Mitochondrial ; Photolysis ; Rats
References:: Br J Pharmacol. 2009 Oct;158(4):1112-20. (PMID: 19785652)
Am J Physiol Heart Circ Physiol. 2011 Feb;300(2):H493-506. (PMID: 21148766)
J Biol Chem. 2014 Mar 21;289(12):8170-81. (PMID: 24469450)
J Biol Chem. 2004 Feb 27;279(9):8417-27. (PMID: 14660609)
Basic Life Sci. 1985;35:75-104. (PMID: 4062824)
J Biol Chem. 1999 May 14;274(20):14157-62. (PMID: 10318833)
J Physiol. 2015 May 1;593(9):2155-69. (PMID: 25689097)
Cardiovasc Res. 2009 Apr 1;82(1):9-20. (PMID: 19179352)
J Physiol. 1999 Apr 1;516 ( Pt 1):149-61. (PMID: 10066930)
Mol Cell. 2007 Apr 13;26(1):1-14. (PMID: 17434122)
J Biol Chem. 2019 Jan 18;294(3):737-758. (PMID: 30498088)
EMBO J. 1999 Nov 15;18(22):6349-61. (PMID: 10562547)
Neuron. 1993 Jun;10(6):1175-84. (PMID: 7686381)
Mol Cell Biochem. 2005 Jan;269(1-2):165-73. (PMID: 15786729)
J Biol Chem. 1996 Dec 27;271(52):33493-501. (PMID: 8969213)
J Physiol. 2000 Nov 15;529 Pt 1:69-81. (PMID: 11080252)
BMC Pharmacol. 2004 May 18;4:6. (PMID: 15149553)
FASEB J. 2000 Apr;14(5):797-804. (PMID: 10744636)
J Physiol. 2012 Aug 1;590(15):3431-47. (PMID: 22855054)
Biochem J. 2013 Apr 15;451(2):177-84. (PMID: 23282150)
Science. 2011 Sep 9;333(6048):1440-5. (PMID: 21903813)
J Biol Chem. 1997 Sep 5;272(36):22654-61. (PMID: 9278423)
Biochem J. 2000 Apr 15;347(Pt 2):593-600. (PMID: 10749691)
Proc Natl Acad Sci U S A. 1990 Mar;87(6):2147-51. (PMID: 2156262)
J Biol Chem. 1993 Aug 25;268(24):17917-23. (PMID: 8394353)
Biochim Biophys Acta. 2004 Jul 9;1657(2-3):105-14. (PMID: 15238267)
Circ Res. 2002 Apr 19;90(7):792-9. (PMID: 11964372)
J Biol Chem. 2004 Mar 26;279(13):12909-17. (PMID: 14699167)
J Biol Chem. 2010 Jan 15;285(3):2040-50. (PMID: 19889626)
J Gen Physiol. 2000 Oct;116(4):547-60. (PMID: 11004204)
Sci Rep. 2015 Nov 23;5:16875. (PMID: 26593883)
Cell Calcium. 1991 Jul;12(7):505-14. (PMID: 1657395)
J Physiol. 2016 Dec 15;594(24):7267-7307. (PMID: 27730645)
Science. 1998 Jun 12;280(5370):1763-6. (PMID: 9624056)
Cell Calcium. 2017 May;63:70-96. (PMID: 28143649)
J Physiol. 2016 Aug 1;594(15):4283-95. (PMID: 26959407)
J Gen Physiol. 1991 Oct;98(4):681-98. (PMID: 1660060)
Curr Top Membr. 2010;66:299-322. (PMID: 22353485)
J Physiol. 2000 Jun 15;525 Pt 3:707-19. (PMID: 10856123)
J Physiol. 2015 Dec 15;593(24):5231-53. (PMID: 26507455)
J Biol Chem. 2001 Jun 29;276(26):23357-61. (PMID: 11283020)
Cold Spring Harb Perspect Med. 2012 Jan;2(1):a006429. (PMID: 22315715)
Cell Calcium. 2009 Aug;46(2):107-13. (PMID: 19577805)
Am J Physiol Lung Cell Mol Physiol. 2015 Dec 15;309(12):L1467-77. (PMID: 26453519)
Cell. 1995 Aug 11;82(3):415-24. (PMID: 7634331)
FASEB J. 1989 Oct;3(12):2389-400. (PMID: 2477294)
Sci Signal. 2018 Dec 18;11(561):. (PMID: 30563865)
J Cell Physiol. 2010 Aug;224(2):334-44. (PMID: 20432430)
J Biol Chem. 2001 Aug 3;276(31):29430-9. (PMID: 11358971)
Mol Cell. 2016 Jul 21;63(2):240-248. (PMID: 27397688)
Ann N Y Acad Sci. 1999;893:269-72. (PMID: 10672246)
J Exp Med. 2000 Oct 2;192(7):1001-14. (PMID: 11015441)
FASEB J. 2003 Jan;17(1):28-37. (PMID: 12522109)
PLoS One. 2012;7(8):e43186. (PMID: 22916222)
Mol Cell. 2012 Oct 26;48(2):158-67. (PMID: 23102266)
Pharmacol Ther. 2018 Dec;192:112-123. (PMID: 30036491)
J Biol Chem. 1985 Nov 25;260(27):14413-6. (PMID: 3877055)
Am J Physiol Cell Physiol. 2004 Oct;287(4):C817-33. (PMID: 15355853)
J Cell Sci. 2003 Nov 1;116(Pt 21):4291-306. (PMID: 12966165)
J Cell Biol. 1999 May 17;145(4):795-808. (PMID: 10330407)
FASEB J. 2016 May;30(5):2000-13. (PMID: 26873937)
J Biol Chem. 1992 Dec 15;267(35):25113-9. (PMID: 1334081)
J Cardiovasc Pharmacol. 2011 Apr;57(4):479-88. (PMID: 21283018)
Trends Pharmacol Sci. 2017 Apr;38(4):322-338. (PMID: 28214012)
J Cell Sci. 2008 Jan 1;121(Pt 1):75-85. (PMID: 18073239)
FASEB J. 2005 May;19(7):837-9. (PMID: 15728661)
J Vasc Res. 2002 May-Jun;39(3):260-7. (PMID: 12097824)
J Cell Biol. 1998 Sep 7;142(5):1235-43. (PMID: 9732284)
Biochem Soc Trans. 2012 Feb;40(1):158-67. (PMID: 22260683)
Proc Natl Acad Sci U S A. 2014 Oct 21;111(42):15250-5. (PMID: 25288763)
Biochem J. 2004 Jul 1;381(Pt 1):87-96. (PMID: 15015936)
Mol Cell Biochem. 1997 Jun;171(1-2):11-21. (PMID: 9201690)
Antioxid Redox Signal. 2013 Mar 20;18(9):1042-52. (PMID: 22867279)
J Neurochem. 2002 Feb;80(3):405-15. (PMID: 11905989)
EMBO J. 2017 Mar 15;36(6):797-815. (PMID: 28219928)
Curr Opin Pharmacol. 2019 Apr;45:23-32. (PMID: 31005824)
J Cell Biol. 2006 Sep 25;174(7):915-21. (PMID: 16982799)
J Biol Chem. 2003 Nov 7;278(45):44735-44. (PMID: 12930841)
Biochem J. 1994 Jan 1;297 ( Pt 1):209-15. (PMID: 8280101)
Proc Natl Acad Sci U S A. 1999 Nov 23;96(24):13807-12. (PMID: 10570154)
Biochim Biophys Acta. 2009 Nov;1787(11):1352-62. (PMID: 19527680)
Circulation. 1998 Jan 27;97(3):268-75. (PMID: 9462529)
Biochim Biophys Acta. 2014 May;1840(5):1596-604. (PMID: 24060746)
Grant Information:: 204682/Z/16/Z United Kingdom WT_ Wellcome Trust; PG/16/54/32230 United Kingdom BHF_ British Heart Foundation; PG/16/82/32439 United Kingdom BHF_ British Heart Foundation
Contributed Indexing:: Keywords: Calcium; Endothelium; Free radical; Hydrogen peroxide; Inositol 1,4,5‐trisphosphate; Vascular
Substance Nomenclature:: 0 (Inositol 1,4,5-Trisphosphate Receptors)
555-60-2 (Carbonyl Cyanide m-Chlorophenyl Hydrazone)
85166-31-0 (Inositol 1,4,5-Trisphosphate)
BBX060AN9V (Hydrogen Peroxide)
N9YNS0M02X (Acetylcholine)
Entry Date(s):: Date Created: 20191113 Date Completed: 20200924 Latest Revision: 20220310
Update Code:: 20240105
PubMed Central ID:: PMC6891240
DOI:: 10.1016/j.ceca.2019.102108
PMID:: 31715384
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Hydrogen peroxide (H 2 O 2 ) is a mitochondrial-derived reactive oxygen species (ROS) that regulates vascular signalling transduction, vasocontraction and vasodilation. Although the physiological role of ROS in endothelial cells is acknowledged, the mechanisms underlying H 2 O 2 regulation of signalling in native, fully-differentiated endothelial cells is unresolved. In the present study, the effects of H 2 O 2 on Ca 2+ signalling were investigated in the endothelium of intact rat mesenteric arteries. Spontaneous local Ca 2+ signals and acetylcholine evoked Ca 2+ increases were inhibited by H 2 O 2 . H 2 O 2 inhibition of acetylcholine-evoked Ca 2+ signals was reversed by catalase. H 2 O 2 exerts its inhibition on the IP 3 receptor as Ca 2+ release evoked by photolysis of caged IP 3 was supressed by H 2 O 2 . H 2 O 2 suppression of IP 3 -evoked Ca 2+ signalling may be mediated by mitochondria. H 2 O 2 depolarized mitochondria membrane potential. Acetylcholine-evoked Ca 2+ release was inhibited by depolarisation of the mitochondrial membrane potential by the uncoupler carbonyl cyanide 3-chlorophenylhydrazone (CCCP) or complex 1 inhibitor, rotenone. We propose that the suppression of IP 3 -evoked Ca 2+ release by H 2 O 2 arises from the decrease in mitochondrial membrane potential. These results suggest that mitochondria may protect themselves against Ca 2+ overload during IP 3 -linked Ca 2+ signals by a H 2 O 2 mediated negative feedback depolarization of the organelle and inhibition of IP 3 -evoked Ca 2+ release.
(Copyright © 2019 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

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Hydrogen peroxide depolarizes mitochondria and inhibits IP 3 -evoked Ca 2+ release in the endothelium of intact arteries.