Details der Publikation - TIMP-2 gene polymorphism is associated with intracerebral hemorrhage

TIMP-2 gene polymorphism is associated with intracerebral hemorrhage / Bjoern Reuter, Peter Bugert, Mark Stroick, Simone Bukow, Martin Griebe, Michael G. Hennerici, Marc Fatar

BACKGROUND: Both ischemic stroke and intracerebral hemorrhage are associated with altered expression and activation of matrix metalloproteinases (MMPs). Particularly relevant are MMP-2 and MMP-9. This proteolytic effect is dampened by tissue inhibitors of metalloproteinases (TIMPs). TIMP-2 is an important endogenous inhibitor of MMP-2. Alterations in the TIMP-2 gene expression may contribute to the incidence of ischemic stroke and intracerebral hemorrhage. - METHODS: TIMP-2 gene SNP -261G/A was genotyped from sequentially recruited stroke patients (n = 356, f/m 151/205, mean age 68.2 years, range 19-100 years) and gender and age matched controls (n = 253, f/m 114/139, mean age 68.5 years, range 32-92 years). The SNP -261G/A was detected after gene sequencing of 95 patients and controls. Furthermore, in a subgroup of 93 patients the serum levels of TIMP-2 were measured during the first 7 days after stroke onset and compared to the genotype. - RESULTS: SNP -261G/A in the TIMP-2 gene shows an allele frequency of approximately 39.14%. Homozygosity for allele A is associated significantly with the development of ICH (p = 0.025, OR = 2.020, CI = 1.115-3.661) as compared to heterozygosity and homozygosity for allele G (recessive genotypic model). Concordantly, the serum levels of TIMP-2 showed a nonsignificant decreases, depending on the genotype (p = 0.111). - CONCLUSION: We investigated a SNP 261 base pairs upstream of the start codon in exon 1 of TIMP-2. Our data suggest that carriers of homozygosity for allele A are at increased risk of developing intracerebral hemorrhage..

Medienart:	E-Artikel

Erscheinungsjahr:	October 16, 2009 2009
Erschienen:	October 16, 2009

Enthalten in:	Zur Gesamtaufnahme - volume:28
Enthalten in:	Cerebrovascular diseases - 28(2009), 6, Seite 558-563

Sprache:	Englisch

Beteiligte Personen:	Reuter, Björn, 1979- [VerfasserIn] Bugert, Peter, 1964- [VerfasserIn] Stroick, Mark Gregor, 1974- [VerfasserIn] Bukow, Simone [VerfasserIn] Griebe, Martin, 1975- [VerfasserIn] Hennerici, Michael G., 1948- [VerfasserIn] Fatar, Marc, 1972- [VerfasserIn]

Links:	Volltext [lizenzpflichtig]

Themen:	Adult Aged Aged, 80 and over Case-Control Studies Cerebral Hemorrhage Female Gene Frequency Genetic Predisposition to Disease Genotype Heterozygote Homozygote Humans Incidence Male Middle Aged Polymorphism, Single Nucleotide Tissue Inhibitor of Metalloproteinase-2

Anmerkungen:	Gesehen am 22.04.2022

Umfang:	6

doi:	10.1159/000247599

funding:
Förderinstitution / Projekttitel:

PPN (Katalog-ID):	1800055641

Internformat


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245	1	0	\|a TIMP-2 gene polymorphism is associated with intracerebral hemorrhage \|c Bjoern Reuter, Peter Bugert, Mark Stroick, Simone Bukow, Martin Griebe, Michael G. Hennerici, Marc Fatar
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520			\|a BACKGROUND: Both ischemic stroke and intracerebral hemorrhage are associated with altered expression and activation of matrix metalloproteinases (MMPs). Particularly relevant are MMP-2 and MMP-9. This proteolytic effect is dampened by tissue inhibitors of metalloproteinases (TIMPs). TIMP-2 is an important endogenous inhibitor of MMP-2. Alterations in the TIMP-2 gene expression may contribute to the incidence of ischemic stroke and intracerebral hemorrhage. - METHODS: TIMP-2 gene SNP -261G/A was genotyped from sequentially recruited stroke patients (n = 356, f/m 151/205, mean age 68.2 years, range 19-100 years) and gender and age matched controls (n = 253, f/m 114/139, mean age 68.5 years, range 32-92 years). The SNP -261G/A was detected after gene sequencing of 95 patients and controls. Furthermore, in a subgroup of 93 patients the serum levels of TIMP-2 were measured during the first 7 days after stroke onset and compared to the genotype. - RESULTS: SNP -261G/A in the TIMP-2 gene shows an allele frequency of approximately 39.14%. Homozygosity for allele A is associated significantly with the development of ICH (p = 0.025, OR = 2.020, CI = 1.115-3.661) as compared to heterozygosity and homozygosity for allele G (recessive genotypic model). Concordantly, the serum levels of TIMP-2 showed a nonsignificant decreases, depending on the genotype (p = 0.111). - CONCLUSION: We investigated a SNP 261 base pairs upstream of the start codon in exon 1 of TIMP-2. Our data suggest that carriers of homozygosity for allele A are at increased risk of developing intracerebral hemorrhage.
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TIMP-2 gene polymorphism is associated with intracerebral hemorrhage / Bjoern Reuter, Peter Bugert, Mark Stroick, Simone Bukow, Martin Griebe, Michael G. Hennerici, Marc Fatar

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