Complement-induced activation of MAPKs and Akt during sepsis: role in cardiac dysfunction.

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Abstrakt

Tytuł:: Complement-induced activation of MAPKs and Akt during sepsis: role in cardiac dysfunction.
Autorzy:: Fattahi F; Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Kalbitz M; Department of Orthopaedic Trauma, Hand, Plastic, and Reconstructive Surgery, University Hospital of Ulm, Ulm, Germany.
Malan EA; Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Abe E; Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Jajou L; Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Huber-Lang MS; Department of Orthopaedic Trauma, Hand, Plastic, and Reconstructive Surgery, University Hospital of Ulm, Ulm, Germany.
Bosmann M; Center for Thrombosis and Hemostasis, University Medical Center, Mainz, Germany.
Russell MW; Department of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Zetoune FS; Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
Ward PA; Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA; .
Źródło:: FASEB journal : official publication of the Federation of American Societies for Experimental Biology [FASEB J] 2017 Sep; Vol. 31 (9), pp. 4129-4139. Date of Electronic Publication: 2017 Jun 01.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't; Research Support, N.I.H., Extramural
Język:: English
Imprint Name(s):: Publication: 2020- : [Bethesda, Md.] : Hoboken, NJ : Federation of American Societies for Experimental Biology ; Wiley
Original Publication: [Bethesda, Md.] : The Federation, [c1987-
MeSH Terms:: Complement C5a/*metabolism
Gene Expression Regulation/*physiology
Heart Diseases/*etiology
Mitogen-Activated Protein Kinase Kinases/*metabolism
Proto-Oncogene Proteins c-akt/*metabolism
Sepsis/*metabolism
Animals ; Complement C5a/genetics ; Heart Diseases/metabolism ; Interleukins ; Male ; Mitogen-Activated Protein Kinase Kinases/genetics ; Proto-Oncogene Proteins c-akt/genetics ; Rats ; Rats, Sprague-Dawley ; Receptor, Anaphylatoxin C5a/genetics ; Receptor, Anaphylatoxin C5a/metabolism
References:: Science. 2002 Dec 6;298(5600):1911-2. (PMID: 12471242)
Circulation. 2001 Sep 11;104(11):1292-8. (PMID: 11551882)
Am J Physiol Heart Circ Physiol. 2001 Mar;280(3):H962-8. (PMID: 11179036)
J Exp Med. 2006 Jan 23;203(1):53-61. (PMID: 16380509)
Crit Care Med. 1999 Jul;27(7):1309-18. (PMID: 10446825)
Am J Physiol Cell Physiol. 2016 Feb 15;310(4):C270-83. (PMID: 26739490)
J Mol Cell Cardiol. 2002 Apr;34(4):413-26. (PMID: 11991731)
Nat Protoc. 2009;4(1):31-6. (PMID: 19131954)
Cell Signal. 2014 Jul;26(7):1409-19. (PMID: 24631530)
Nat Rev Drug Discov. 2003 Sep;2(9):717-26. (PMID: 12951578)
Am J Physiol Heart Circ Physiol. 2003 Oct;285(4):H1506-14. (PMID: 12805025)
Crit Care Med. 2008 Feb;36(2):482-8. (PMID: 18091546)
Clin Exp Pharmacol Physiol. 2008 Feb;35(2):126-34. (PMID: 17892505)
Mol Immunol. 2017 Apr;84:57-64. (PMID: 27931779)
Apoptosis. 2014 Apr;19(4):567-80. (PMID: 24248985)
J Innate Immun. 2017;9(3):300-317. (PMID: 28171866)
Res Commun Chem Pathol Pharmacol. 1994 May;84(2):189-95. (PMID: 8091004)
Ann Surg. 2005 Dec;242(6):830-8, discussion 838-9. (PMID: 16327493)
Crit Care Res Pract. 2012;2012:427607. (PMID: 22482043)
Crit Care Med. 2001 Mar;29(3):503-10. (PMID: 11373411)
Nature. 2007 Mar 8;446(7132):203-7. (PMID: 17322907)
FASEB J. 2011 Dec;25(12):4222-32. (PMID: 21859896)
FASEB J. 2004 Feb;18(2):370-2. (PMID: 14688199)
N Engl J Med. 1996 Jun 27;334(26):1697-702. (PMID: 8637514)
Cardiovasc Res. 2004 Feb 15;61(3):427-36. (PMID: 14962474)
FASEB J. 2016 Dec;30(12 ):3997-4006. (PMID: 27543123)
Cell Health Cytoskelet. 2012 Jul 1;4:73-82. (PMID: 23576881)
J Immunol. 2014 Jun 15;192(12 ):5974-83. (PMID: 24795455)
J Clin Oncol. 2013 May 10;31(14 ):1767-74. (PMID: 23569304)
Nat Med. 2008 May;14(5):551-7. (PMID: 18454156)
J Biol Chem. 1994 Aug 5;269(31):19947-52. (PMID: 8051079)
Nat Commun. 2016 Mar 18;7:10879. (PMID: 26988444)
Arthritis Rheum. 2000 Jan;43(1):175-83. (PMID: 10643714)
J Immunol. 2007 May 1;178(9):5940-8. (PMID: 17442978)
FASEB J. 2013 Dec;27(12):5010-21. (PMID: 23982144)
FASEB J. 2012 Apr;26(4):1640-51. (PMID: 22202675)
J Immunol. 2001 Jan 15;166(2):1193-9. (PMID: 11145701)
J Biol Chem. 2003 Jan 24;278(4):2118-23. (PMID: 12431978)
Nature. 1996 Sep 5;383(6595):86-9. (PMID: 8779720)
Curr Biol. 1998 Sep 24;8(19):1049-57. (PMID: 9768359)
J Biol Chem. 1999 Oct 22;274(43):30349-52. (PMID: 10521408)
Crit Care. 2008;12(6):R158. (PMID: 19091069)
J Invest Surg. 2004 Nov-Dec;17(6):303-13. (PMID: 15764497)
Intensive Care Med. 1999 Oct;25(10):1165-8. (PMID: 10551977)
J Biol Chem. 2005 Dec 2;280(48):39677-80. (PMID: 16204243)
FASEB J. 2001 Mar;15(3):568-70. (PMID: 11259369)
Eur J Pharmacol. 2017 Feb 5;796:90-100. (PMID: 27916558)
Biochem J. 2013 Dec 1;456(2):149-61. (PMID: 24032640)
J Mol Cell Cardiol. 1999 Aug;31(8):1429-34. (PMID: 10423341)
Curr Cardiol Rev. 2011 Aug;7(3):163-83. (PMID: 22758615)
Curr Opin Cardiol. 2013 May;28(3):297-304. (PMID: 23455585)
FASEB J. 2015 May;29(5):2185-93. (PMID: 25681459)
Biochem Biophys Res Commun. 2000 Apr 21;270(3):947-52. (PMID: 10772931)
J Immunol. 2016 Sep 15;197(6):2353-61. (PMID: 27521340)
J Biomol Struct Dyn. 2014;32(7):1047-63. (PMID: 23805842)
Basic Res Cardiol. 2014 Jul;109(4):420. (PMID: 24951957)
Nat Rev Immunol. 2007 Mar;7(3):202-12. (PMID: 17318231)
Grant Information:: R01 GM029507 United States GM NIGMS NIH HHS; R01 GM061656 United States GM NIGMS NIH HHS; R37 GM029507 United States GM NIGMS NIH HHS
Contributed Indexing:: Keywords: C5a receptor; CLP; cardiomyocyte
Substance Nomenclature:: 0 (C5ar1 protein, mouse)
0 (C5ar2 protein, mouse)
0 (Interleukins)
0 (Receptor, Anaphylatoxin C5a)
80295-54-1 (Complement C5a)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
Entry Date(s):: Date Created: 20170603 Date Completed: 20171013 Latest Revision: 20181113
Update Code:: 20240104
PubMed Central ID:: PMC5572692
DOI:: 10.1096/fj.201700140R
PMID:: 28572445
: Czasopismo naukowe

Polymicrobial sepsis in mice causes myocardial dysfunction after generation of the complement anaphylatoxin, complement component 5a (C5a). C5a interacts with its receptors on cardiomyocytes (CMs), resulting in redox imbalance and cardiac dysfunction that can be functionally measured and quantitated using Doppler echocardiography. In this report we have evaluated activation of MAPKs and Akt in CMs exposed to C5a in vitro and after cecal ligation and puncture (CLP) in vivo In both cases, C5a in vitro caused activation (phosphorylation) of MAPKs and Akt in CMs, which required availability of both C5a receptors. Using immunofluorescence technology, activation of MAPKs and Akt occurred in left ventricular (LV) CMs, requiring both C5a receptors, C5aR1 and -2. Use of a water-soluble p38 inhibitor curtailed activation in vivo of MAPKs and Akt in LV CMs as well as the appearance of cytokines and histones in plasma from CLP mice. When mouse macrophages were exposed in vitro to LPS, activation of MAPKs and Akt also occurred. The copresence of the p38 inhibitor blocked these activation responses. Finally, the presence of the p38 inhibitor in CLP mice reduced the development of cardiac dysfunction. These data suggest that polymicrobial sepsis causes cardiac dysfunction that appears to be linked to activation of MAPKs and Akt in heart.-Fattahi, F., Kalbitz, M., Malan, E. A., Abe, E., Jajou, L., Huber-Lang, M. S., Bosmann, M., Russell, M. W., Zetoune, F. S., Ward, P. A. Complement-induced activation of MAPKs and Akt during sepsis: role in cardiac dysfunction.
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