Association of polymorphisms of zinc metalloproteinases with clinical response to stem cell therapy
Jazyk angličtina Země Německo Médium print
Typ dokumentu srovnávací studie, časopisecké články, randomizované kontrolované studie, práce podpořená grantem
- MeSH
- alely MeSH
- angiotensin konvertující enzym genetika MeSH
- frekvence genu genetika MeSH
- funkce levé komory srdeční fyziologie MeSH
- genotyp * MeSH
- infarkt myokardu genetika patofyziologie terapie MeSH
- kontrakce myokardu fyziologie MeSH
- lidé MeSH
- matrixová metaloproteinasa 2 genetika MeSH
- počet buněk MeSH
- polymerázová řetězová reakce MeSH
- polymorfismus genetický genetika MeSH
- promotorové oblasti (genetika) genetika MeSH
- stenty MeSH
- transplantace kostní dřeně * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- randomizované kontrolované studie MeSH
- srovnávací studie MeSH
- Názvy látek
- angiotensin konvertující enzym MeSH
- matrixová metaloproteinasa 2 MeSH
- MMP2 protein, human MeSH Prohlížeč
AIM: The purpose of this study was to assess the associations of polymorphisms in two metalloproteinase genes-metalloproteinase-2 (MMP-2) and angiotensin converting enzyme (ACE)-with clinical response to autologous transplantation of mononuclear bone marrow cells (MBMC) in patients with acute myocardial infarction. METHODS: The double centre study included 48 patients with a first acute myocardial infarction treated with primary coronary angioplasty, stent implantation and transplantation of MBMC. According to the changes in perfusion defect size, left ventricle ejection fraction, end-systolic volume and peak systolic velocity of the infracted wall (dSaMI) after cell therapy, the patients were retrospectively divided into group A (responders) and group B (non-responders). Genomic DNA was isolated from peripheral leukocytes by a standard technique using proteinase K. Three MMP-2 promoter (-1575G/A, -1306C/T and -790T/G) as well as I/D ACE gene polymorphisms were detected by PCR methods with restriction analyses (when necessary) according to standard protocols. RESULTS: Of the 48 patients who received MBMC transplantation, 17 responded to the therapy. There were no significant differences in the prevalence of matrix metalloproteinase-2 triple genotype GGCCTT between responder/non-responder groups (71% versus 61%, p=0.375). Similarly, no differences in either genotype distribution or allelic frequencies of I/D ACE polymorphism between responders and non-responders to the cell therapy were observed (p=0.933). Compared to patients with ACE genotype ID or DD, the patients with ACE II genotype significantly improved in regional systolic LV function of the infarcted wall after implantations of MBMC (dSaMI - 0.4 versus 1.4 cm/s, p=0.037). CONCLUSION: In our study, the ACE genotype II was associated with improvement of regional systolic LV function of the infarcted wall after implantations of MBMC. The detected polymorphism in matrix metalloproteinase-2 gene was not associated with clinical response to cell therapy.
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Eur J Heart Fail. 2007 Aug;9(8):747-53 PubMed
J Thorac Cardiovasc Surg. 2005 Nov;130(5):1430-9 PubMed
Int J Cardiol. 2005 Nov 2;105(2):203-8 PubMed
Cardiovasc Res. 2006 Feb 15;69(3):604-13 PubMed
Lancet. 2000 Feb 5;355(9202):434-42 PubMed
Circulation. 2005 Apr 12;111(14):1800-5 PubMed
J Card Fail. 2004 Aug;10(4):328-33 PubMed
Eur J Heart Fail. 2008 Nov;10(11):1065-72 PubMed
Cardiovasc Res. 2006 Feb 1;69(2):476-90 PubMed
J Am Coll Cardiol. 2002 Jul 3;40(1):43-8 PubMed
Circ Res. 2001 Aug 3;89(3):201-10 PubMed
Circ Res. 2004 Mar 19;94(5):678-85 PubMed
Circulation. 1996 Aug 15;94(4):708-12 PubMed
Eur J Heart Fail. 2000 Sep;2(3):253-6 PubMed
Am Heart J. 2007 Apr;153(4):641-8 PubMed
Semin Thorac Cardiovasc Surg. 2008 Summer;20(2):94-101 PubMed
Clin Genet. 2002 Jan;61(1):21-5 PubMed
Eur Heart J. 2004 Apr;25(8):688-93 PubMed
Circulation. 1999 Jun 15;99(23):3063-70 PubMed
Am Heart J. 2006 Nov;152(5):975.e9-15 PubMed
Am J Physiol Heart Circ Physiol. 2003 Sep;285(3):H1229-35 PubMed
J Am Coll Cardiol. 1995 Jun;25(7):1622-6 PubMed
Jpn Circ J. 2001 Sep;65(9):845-7 PubMed
J Nucl Cardiol. 2008 May-Jun;15(3):392-9 PubMed
Circulation. 2005 Aug 30;112(9 Suppl):I178-83 PubMed
Int J Cardiol. 1999 Jul 31;70(2):119-25 PubMed
Cardiovasc Res. 2005 Apr 1;66(1):22-32 PubMed
J Card Fail. 2006 Feb;12(1):66-72 PubMed
Echocardiography. 2008 Sep;25(8):888-97 PubMed
Lancet. 2003 Jan 4;361(9351):45-6 PubMed
Eur Heart J. 2007 Mar;28(6):659-60 PubMed
Matrix Biol. 2004 Jan;22(7):585-91 PubMed
J Clin Invest. 2005 Mar;115(3):599-609 PubMed
Eur Heart J. 2007 Mar;28(6):711-8 PubMed
Cell Transplant. 2004;13(1):7-13 PubMed
J Am Coll Cardiol. 1998 Aug;32(2):368-72 PubMed
Clin Sci (Lond). 2007 Jan;112(1):43-9 PubMed
Clin Cardiol. 1999 Sep;22(9):587-90 PubMed
Circ Res. 2006 Jun 9;98(11):1414-21 PubMed
Cell Transplant. 2007;16(4):365-74 PubMed
Circ Res. 2004 Oct 1;95(7):742-8 PubMed
Int J Cardiol. 1996 Mar;53(3):265-72 PubMed
Circulation. 2003 Feb 4;107(4):618-25 PubMed
J Card Fail. 2007 Dec;13(10):843-9 PubMed
N Engl J Med. 2006 Sep 21;355(12):1199-209 PubMed
J Am Coll Cardiol. 2003 May 21;41(10):1721-4 PubMed
Lancet. 2003 Jan 4;361(9351):47-9 PubMed