Downregulation of myogenic microRNAs in sub-chronic but not in sub-acute model of daunorubicin-induced cardiomyopathy
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
28303410
DOI
10.1007/s11010-017-2999-8
PII: 10.1007/s11010-017-2999-8
Knihovny.cz E-zdroje
- Klíčová slova
- Anthracycline, Cardiomyopathy, Gene expression, MicroRNA, Myosin heavy chain isoforms, NADPH oxidase,
- MeSH
- daunomycin škodlivé účinky farmakologie MeSH
- down regulace účinky léků MeSH
- kardiomyopatie chemicky indukované metabolismus patologie patofyziologie MeSH
- krysa rodu Rattus MeSH
- mikro RNA biosyntéza MeSH
- modely nemocí na zvířatech MeSH
- potkani Wistar MeSH
- svalové proteiny biosyntéza MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- daunomycin MeSH
- mikro RNA MeSH
- svalové proteiny MeSH
Cardiac muscle-related microRNAs play important roles in cardiac development and disease by translational silencing of mRNAs, the dominant mechanism of microRNA action. To test whether they could be involved in daunorubicin-associated cardiomyopathy (DACM), we determined expression patterns of myomiRs in two distinct models of DACM. We used 10-12 weeks old male Wistar rats. In the sub-acute model, rats were administered with six doses of daunorubicin (DAU-A, 3 mg/kg, i.p., every 48 h). Rats were sacrificed two days after the last dose. In the sub-chronic model, anaesthetized rats were administered a single dose of daunorubicin (15 mg/kg, i.v., DAU-C). Age-matched controls (CON) received vehicle. Rats were sacrificed eight weeks later. Left ventricular (LV) functions (LV pressure, rate of pressure development, +dP/dt and decline, -dP/dt) were measured using left ventricular catheterization. Expressions of myomiRs (miR-208a, miR-499, miR-1 and miR-133a), markers of cardiac failure (atrial and brain natriuretic peptides genes; Nppa and Nppb) and myosin heavy chain genes (Myh6, Myh7, Myh7b) in cardiac tissue were determined by RT-PCR. Protein expression of gp91phox NADPH oxidase subunit was detected by immunoblotting. Both DAU groups exhibited a similar depression of LV function, and LV weight reduction, accompanied by an upregulation of natriuretic peptides, and a decrease of Myh6 to total Myh ratio (-18% in DAU-A and - 25% in DAU-C, as compared to controls; both P < 0.05). DAU-C, but not DAU-A rats had a 35% mortality rate and exhibited a significantly increased gp91phox expression (DAU-C: 197 ± 33 versus CON-C: 100 ± 11; P < 0.05). Interestingly, myomiRs levels were only reduced in DAU-C compared to CON-C (miR-208: -45%, miR-499: -30%, miR-1: -29%, miR- and miR133a: -25%; all P < 0.05) but were unaltered in DAU-A. The lack of myomiRs expression, particularly in sub-chronic model, suggests the loss of control of myomiRs network on late progression of DACM. We suppose that the poor inhibition of mRNA targets might contribute to chronic DACM.
Zobrazit více v PubMed
Nucleic Acids Res. 2012 Aug;40(15):7303-18 PubMed
Cancer Res. 2010 Nov 15;70(22):9287-97 PubMed
Eur J Pharmacol. 2010 Sep 1;641(2-3):187-92 PubMed
Am J Physiol Heart Circ Physiol. 2008 Feb;294(2):H1048-57 PubMed
Circulation. 2011 Oct 4;124(14 ):1537-47 PubMed
J Pharmacol Exp Ther. 2011 Dec;339(3):807-14 PubMed
Cell Death Dis. 2015 May 07;6:e1754 PubMed
PLoS One. 2011 May 09;6(5):e19481 PubMed
Circulation. 2006 Jan 31;113(4):535-43 PubMed
Am J Pathol. 1984 Oct;117(1):140-53 PubMed
J Clin Invest. 2013 Jul;123(7):2921-34 PubMed
Med Sci Sports Exerc. 2008 May;40(5):808-17 PubMed
Proc Natl Acad Sci U S A. 2014 Jul 29;111(30):11151-6 PubMed
Nat Med. 2011 Jan;17(1):71-8 PubMed
Circ Res. 2008 Oct 24;103(9):919-28 PubMed
Am J Physiol Heart Circ Physiol. 2015 Sep;309(5):H844-59 PubMed
Am J Pathol. 2007 Jun;170(6):1831-40 PubMed
PLoS One. 2014 May 07;9(5):e96055 PubMed
Circ Heart Fail. 2015 Jan;8(1):98-108 PubMed
Circ Res. 2009 Jan 30;104(2):170-8, 6p following 178 PubMed
J Clin Invest. 2009 Sep;119(9):2772-86 PubMed
Mol Cell Biochem. 2015 Jun;404(1-2):45-51 PubMed
Antioxid Redox Signal. 2013 Mar 10;18(8):899-929 PubMed
Clin Sci (Lond). 2008 Jun;114(12):699-706 PubMed
J Mol Cell Cardiol. 2007 Oct;43(4):388-403 PubMed
Clin Exp Pharmacol Physiol. 2014 Sep;41(9):727-37 PubMed
J Cell Sci. 2007 Sep 1;120(Pt 17):3045-52 PubMed
Cardiovasc Res. 2008 Sep 1;79(4):562-70 PubMed
Mol Pharmacol. 2000 Jun;57(6):1152-7 PubMed
Dev Cell. 2009 Nov;17(5):662-73 PubMed
Toxicology. 2006 Mar 15;220(2-3):160-8 PubMed
Toxicol Appl Pharmacol. 2015 Apr 15;284(2):152-62 PubMed
Pharmacol Rev. 2004 Jun;56(2):185-229 PubMed
Toxicol Appl Pharmacol. 2014 Dec 1;281(2):221-9 PubMed
J Biol Chem. 2003 May 9;278(19):17466-74 PubMed
Basic Clin Pharmacol Toxicol. 2015 Oct;117(4):251-60 PubMed
Dev Cell. 2010 Apr 20;18(4):510-25 PubMed
Circ Res. 2007 Feb 16;100(3):416-24 PubMed
Science. 2007 Apr 27;316(5824):575-9 PubMed
Circ Res. 2007 Dec 7;101(12):1225-36 PubMed
Nature. 2005 Jul 14;436(7048):214-20 PubMed
Am J Physiol Heart Circ Physiol. 2009 Jul;297(1):H37-46 PubMed
PLoS One. 2012;7(7):e40395 PubMed
Cardiovasc Toxicol. 2001;1(4):267-83 PubMed
Am J Transl Res. 2015 Jul 15;7(7):1280-94 PubMed
J Cardiol. 2013 Aug;62(2):110-6 PubMed
Am J Pathol. 2010 Feb;176(2):687-98 PubMed
Pharmacol Rep. 2009 Jan-Feb;61(1):154-71 PubMed
Nat Med. 2007 May;13(5):613-8 PubMed
Mol Cell Biol. 2009 Apr;29(8):2193-204 PubMed
Toxicology. 1996 Nov 15;114(1):1-10 PubMed
Circ Cardiovasc Genet. 2010 Oct;3(5):426-35 PubMed
Nucleic Acids Res. 2009 Apr;37(6):e45 PubMed