Genetic polymorphisms of UTS2 rs2890565 Ser89Asn in cardiac hypertrophy in Chinese Han population
ObjectiveCardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli, some of which might finally lead up to a maladaptive state. Clinical evidence, in vitro and in vivo studies have implicated urotensin II (U-II/UTS2) in the development of cardiac hypertrophy, c...
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| Veröffentlicht in: | Postgraduate medical journal Jg. 93; H. 1101; S. 406 - 413 |
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01.07.2017
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| Abstract | ObjectiveCardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli, some of which might finally lead up to a maladaptive state. Clinical evidence, in vitro and in vivo studies have implicated urotensin II (U-II/UTS2) in the development of cardiac hypertrophy, contributing to the (patho)-physiological regulation of cardiovascular homeostasis in humans. Several genes are associated with left ventricular hypertrophy; considering these, our objective was to evaluate the possible role of UTS2 gene polymorphisms (Thr21Met and Ser89Asn) in the genetic susceptibility to cardiac hypertrophy in a Chinese population.MethodsA case-control study was designed to compare the distribution of alleles and genotypes between three groups: case group 1 (subjects with hypertension and cardiac hypertrophy, n=265), case group 2 (subjects with hypertension, without cardiac hypertrophy, n=768), and the control group (subjects neither with hypertension nor with cardiac hypertrophy, n=416). The detection of UTS2 gene polymorphisms was achieved with the PCR restriction fragment length polymorphism technique.ResultsWe did not identify statistically significant differences between the three groups, neither with regard to the frequency of genotype/variant at the Ser89Asn locus nor at the Thr21Met locus. When stratified by sex, differences in genotype distribution of polymorphism Ser89Asn were only seen in female subjects in both the additive tested inheritance model (OR=0.507, 95% CI 0.249 to 1.032, p=0.032) and the recessive tested inheritance model (OR=0.475, 95% CI 0.239 to 0.945, p=0.034) between case group 2 (subjects with hypertension, without cardiac hypertrophy) and the control group (subjects neither with hypertension nor with cardiac hypertrophy). When stratified by sex, for female subjects with cardiac hypertrophy, we identified statistically significant differences in left ventricular posterior wall thickness for variant genotypes at the Ser89Asn locus (AA vs GG: 1.2500 (1.2000, 1.3750) vs 1.2500 (1.2000, 1.3750), p=0.03) and (AG+AA vs GG: 1.2000 (1.2000, 1.3000) vs 1.2000 (1.1000, 1.2000), p=0.01).ConclusionsSer89Asn (S89N) polymorphisms of the UTS2 gene were associated with hypertension in a Chinese female population. Additionally, we demonstrated that genotype Asn89Asn was associated with left ventricular posterior wall thickness for subjects with hypertension and cardiac hypertrophy in a Chinese female population. |
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| AbstractList | ObjectiveCardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli, some of which might finally lead up to a maladaptive state. Clinical evidence, in vitro and in vivo studies have implicated urotensin II (U-II/UTS2) in the development of cardiac hypertrophy, contributing to the (patho)-physiological regulation of cardiovascular homeostasis in humans. Several genes are associated with left ventricular hypertrophy; considering these, our objective was to evaluate the possible role of UTS2 gene polymorphisms (Thr21Met and Ser89Asn) in the genetic susceptibility to cardiac hypertrophy in a Chinese population.MethodsA case-control study was designed to compare the distribution of alleles and genotypes between three groups: case group 1 (subjects with hypertension and cardiac hypertrophy, n=265), case group 2 (subjects with hypertension, without cardiac hypertrophy, n=768), and the control group (subjects neither with hypertension nor with cardiac hypertrophy, n=416). The detection of UTS2 gene polymorphisms was achieved with the PCR restriction fragment length polymorphism technique.ResultsWe did not identify statistically significant differences between the three groups, neither with regard to the frequency of genotype/variant at the Ser89Asn locus nor at the Thr21Met locus. When stratified by sex, differences in genotype distribution of polymorphism Ser89Asn were only seen in female subjects in both the additive tested inheritance model (OR=0.507, 95% CI 0.249 to 1.032, p=0.032) and the recessive tested inheritance model (OR=0.475, 95% CI 0.239 to 0.945, p=0.034) between case group 2 (subjects with hypertension, without cardiac hypertrophy) and the control group (subjects neither with hypertension nor with cardiac hypertrophy). When stratified by sex, for female subjects with cardiac hypertrophy, we identified statistically significant differences in left ventricular posterior wall thickness for variant genotypes at the Ser89Asn locus (AA vs GG: 1.2500 (1.2000, 1.3750) vs 1.2500 (1.2000, 1.3750), p=0.03) and (AG+AA vs GG: 1.2000 (1.2000, 1.3000) vs 1.2000 (1.1000, 1.2000), p=0.01).ConclusionsSer89Asn (S89N) polymorphisms of the UTS2 gene were associated with hypertension in a Chinese female population. Additionally, we demonstrated that genotype Asn89Asn was associated with left ventricular posterior wall thickness for subjects with hypertension and cardiac hypertrophy in a Chinese female population. Objective Cardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli, some of which might finally lead up to a maladaptive state. Clinical evidence, in vitro and in vivo studies have implicated urotensin II (U-II/UTS2) in the development of cardiac hypertrophy, contributing to the (patho)-physiological regulation of cardiovascular homeostasis in humans. Several genes are associated with left ventricular hypertrophy; considering these, our objective was to evaluate the possible role of UTS2 gene polymorphisms (Thr21Met and Ser89Asn) in the genetic susceptibility to cardiac hypertrophy in a Chinese population. Methods A case-control study was designed to compare the distribution of alleles and genotypes between three groups: case group 1 (subjects with hypertension and cardiac hypertrophy, n=265), case group 2 (subjects with hypertension, without cardiac hypertrophy, n=768), and the control group (subjects neither with hypertension nor with cardiac hypertrophy, n=416). The detection of UTS2 gene polymorphisms was achieved with the PCR restriction fragment length polymorphism technique. Results We did not identify statistically significant differences between the three groups, neither with regard to the frequency of genotype/variant at the Ser89Asn locus nor at the Thr21Met locus. When stratified by sex, differences in genotype distribution of polymorphism Ser89Asn were only seen in female subjects in both the additive tested inheritance model (OR=0.507, 95% CI 0.249 to 1.032, p=0.032) and the recessive tested inheritance model (OR=0.475, 95% CI 0.239 to 0.945, p=0.034) between case group 2 (subjects with hypertension, without cardiac hypertrophy) and the control group (subjects neither with hypertension nor with cardiac hypertrophy). When stratified by sex, for female subjects with cardiac hypertrophy, we identified statistically significant differences in left ventricular posterior wall thickness for variant genotypes at the Ser89Asn locus (AA vs GG: 1.2500 (1.2000, 1.3750) vs 1.2500 (1.2000, 1.3750), p=0.03) and (AG+AA vs GG: 1.2000 (1.2000, 1.3000) vs 1.2000 (1.1000, 1.2000), p=0.01). Conclusions Ser89Asn (S89N) polymorphisms of the UTS2 gene were associated with hypertension in a Chinese female population. Additionally, we demonstrated that genotype Asn89Asn was associated with left ventricular posterior wall thickness for subjects with hypertension and cardiac hypertrophy in a Chinese female population. Cardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli, some of which might finally lead up to a maladaptive state. Clinical evidence, in vitro and in vivo studies have implicated urotensin II (U-II/UTS2) in the development of cardiac hypertrophy, contributing to the (patho)-physiological regulation of cardiovascular homeostasis in humans. Several genes are associated with left ventricular hypertrophy; considering these, our objective was to evaluate the possible role of UTS2 gene polymorphisms (Thr21Met and Ser89Asn) in the genetic susceptibility to cardiac hypertrophy in a Chinese population.OBJECTIVECardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli, some of which might finally lead up to a maladaptive state. Clinical evidence, in vitro and in vivo studies have implicated urotensin II (U-II/UTS2) in the development of cardiac hypertrophy, contributing to the (patho)-physiological regulation of cardiovascular homeostasis in humans. Several genes are associated with left ventricular hypertrophy; considering these, our objective was to evaluate the possible role of UTS2 gene polymorphisms (Thr21Met and Ser89Asn) in the genetic susceptibility to cardiac hypertrophy in a Chinese population.A case-control study was designed to compare the distribution of alleles and genotypes between three groups: case group 1 (subjects with hypertension and cardiac hypertrophy, n=265), case group 2 (subjects with hypertension, without cardiac hypertrophy, n=768), and the control group (subjects neither with hypertension nor with cardiac hypertrophy, n=416). The detection of UTS2 gene polymorphisms was achieved with the PCR restriction fragment length polymorphism technique.METHODSA case-control study was designed to compare the distribution of alleles and genotypes between three groups: case group 1 (subjects with hypertension and cardiac hypertrophy, n=265), case group 2 (subjects with hypertension, without cardiac hypertrophy, n=768), and the control group (subjects neither with hypertension nor with cardiac hypertrophy, n=416). The detection of UTS2 gene polymorphisms was achieved with the PCR restriction fragment length polymorphism technique.We did not identify statistically significant differences between the three groups, neither with regard to the frequency of genotype/variant at the Ser89Asn locus nor at the Thr21Met locus. When stratified by sex, differences in genotype distribution of polymorphism Ser89Asn were only seen in female subjects in both the additive tested inheritance model (OR=0.507, 95% CI 0.249 to 1.032, p=0.032) and the recessive tested inheritance model (OR=0.475, 95% CI 0.239 to 0.945, p=0.034) between case group 2 (subjects with hypertension, without cardiac hypertrophy) and the control group (subjects neither with hypertension nor with cardiac hypertrophy). When stratified by sex, for female subjects with cardiac hypertrophy, we identified statistically significant differences in left ventricular posterior wall thickness for variant genotypes at the Ser89Asn locus (AA vs GG: 1.2500 (1.2000, 1.3750) vs 1.2500 (1.2000, 1.3750), p=0.03) and (AG+AA vs GG: 1.2000 (1.2000, 1.3000) vs 1.2000 (1.1000, 1.2000), p=0.01).RESULTSWe did not identify statistically significant differences between the three groups, neither with regard to the frequency of genotype/variant at the Ser89Asn locus nor at the Thr21Met locus. When stratified by sex, differences in genotype distribution of polymorphism Ser89Asn were only seen in female subjects in both the additive tested inheritance model (OR=0.507, 95% CI 0.249 to 1.032, p=0.032) and the recessive tested inheritance model (OR=0.475, 95% CI 0.239 to 0.945, p=0.034) between case group 2 (subjects with hypertension, without cardiac hypertrophy) and the control group (subjects neither with hypertension nor with cardiac hypertrophy). When stratified by sex, for female subjects with cardiac hypertrophy, we identified statistically significant differences in left ventricular posterior wall thickness for variant genotypes at the Ser89Asn locus (AA vs GG: 1.2500 (1.2000, 1.3750) vs 1.2500 (1.2000, 1.3750), p=0.03) and (AG+AA vs GG: 1.2000 (1.2000, 1.3000) vs 1.2000 (1.1000, 1.2000), p=0.01).Ser89Asn (S89N) polymorphisms of the UTS2 gene were associated with hypertension in a Chinese female population. Additionally, we demonstrated that genotype Asn89Asn was associated with left ventricular posterior wall thickness for subjects with hypertension and cardiac hypertrophy in a Chinese female population.CONCLUSIONSSer89Asn (S89N) polymorphisms of the UTS2 gene were associated with hypertension in a Chinese female population. Additionally, we demonstrated that genotype Asn89Asn was associated with left ventricular posterior wall thickness for subjects with hypertension and cardiac hypertrophy in a Chinese female population. Cardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli, some of which might finally lead up to a maladaptive state. Clinical evidence, in vitro and in vivo studies have implicated urotensin II (U-II/UTS2) in the development of cardiac hypertrophy, contributing to the (patho)-physiological regulation of cardiovascular homeostasis in humans. Several genes are associated with left ventricular hypertrophy; considering these, our objective was to evaluate the possible role of UTS2 gene polymorphisms (Thr21Met and Ser89Asn) in the genetic susceptibility to cardiac hypertrophy in a Chinese population. A case-control study was designed to compare the distribution of alleles and genotypes between three groups: case group 1 (subjects with hypertension and cardiac hypertrophy, n=265), case group 2 (subjects with hypertension, without cardiac hypertrophy, n=768), and the control group (subjects neither with hypertension nor with cardiac hypertrophy, n=416). The detection of UTS2 gene polymorphisms was achieved with the PCR restriction fragment length polymorphism technique. We did not identify statistically significant differences between the three groups, neither with regard to the frequency of genotype/variant at the Ser89Asn locus nor at the Thr21Met locus. When stratified by sex, differences in genotype distribution of polymorphism Ser89Asn were only seen in female subjects in both the additive tested inheritance model (OR=0.507, 95% CI 0.249 to 1.032, p=0.032) and the recessive tested inheritance model (OR=0.475, 95% CI 0.239 to 0.945, p=0.034) between case group 2 (subjects with hypertension, without cardiac hypertrophy) and the control group (subjects neither with hypertension nor with cardiac hypertrophy). When stratified by sex, for female subjects with cardiac hypertrophy, we identified statistically significant differences in left ventricular posterior wall thickness for variant genotypes at the Ser89Asn locus (AA vs GG: 1.2500 (1.2000, 1.3750) vs 1.2500 (1.2000, 1.3750), p=0.03) and (AG+AA vs GG: 1.2000 (1.2000, 1.3000) vs 1.2000 (1.1000, 1.2000), p=0.01). Ser89Asn (S89N) polymorphisms of the UTS2 gene were associated with hypertension in a Chinese female population. Additionally, we demonstrated that genotype Asn89Asn was associated with left ventricular posterior wall thickness for subjects with hypertension and cardiac hypertrophy in a Chinese female population. |
| Author | Xue, Lin Ding, Wen-Hui Han, Xiao-Ning Zhao, Jing Chu, Song-Yun Jiang, Jie Wang, Jie Liu, Lin |
| Author_xml | – sequence: 1 givenname: Jing surname: Zhao fullname: Zhao, Jing email: dwh_rd@126.com – sequence: 2 givenname: Jie surname: Jiang fullname: Jiang, Jie email: dwh_rd@126.com – sequence: 3 givenname: Jie surname: Wang fullname: Wang, Jie email: dwh_rd@126.com – sequence: 4 givenname: Lin surname: Liu fullname: Liu, Lin email: dwh_rd@126.com – sequence: 5 givenname: Xiao-Ning surname: Han fullname: Han, Xiao-Ning email: dwh_rd@126.com – sequence: 6 givenname: Song-Yun surname: Chu fullname: Chu, Song-Yun email: dwh_rd@126.com – sequence: 7 givenname: Lin surname: Xue fullname: Xue, Lin email: dwh_rd@126.com – sequence: 8 givenname: Wen-Hui surname: Ding fullname: Ding, Wen-Hui email: dwh_rd@126.com |
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| CitedBy_id | crossref_primary_10_1016_j_drudis_2019_08_005 crossref_primary_10_1016_j_genrep_2020_100789 crossref_primary_10_1007_s11033_025_10662_5 |
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| Keywords | single nucleotide polymorphisms (SNP) cardiac hypertrophy hypertension urotensin-II (U-II/UTS-II) |
| Language | English |
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Wall stress in the normal and hypertrophied human left ventricle publication-title: Am J Cardiol doi: 10.1016/0002-9149(68)90161-6 – volume: 25 start-page: 1783 year: 2004 ident: 2023041308192708500_ article-title: Cardiovascular role of urotensin II: effect of chronic infusion in the rat publication-title: Peptides doi: 10.1016/j.peptides.2004.03.029 – volume: 65 start-page: 501 year: 1963 ident: 2023041308192708500_ article-title: Quantitation of valvular insufficiency in man by angiocardiography publication-title: Am Heart J doi: 10.1016/0002-8703(63)90100-5 – volume: 18 start-page: 2344 year: 2004 ident: 2023041308192708500_ article-title: Urotensin II promotes hypertrophy of cardiac myocytes via mitogen-activated protein kinases publication-title: Mol Endocrinol doi: 10.1210/me.2003-0309 – volume: 2 start-page: 38 year: 2011 ident: 2023041308192708500_ article-title: Potential clinical implications of the Urotensin II Receptor Antagonists publication-title: Front Pharmacol doi: 10.3389/fphar.2011.00038 – volume: 7 start-page: 589 year: 2006 ident: 2023041308192708500_ article-title: Regulation of cardiac hypertrophy by intracellular signalling pathways publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm1983 – volume: 150 start-page: 192 year: 2007 ident: 2023041308192708500_ article-title: Prolonged QTc intervals and decreased left ventricular contractility in patients with propionic acidemia publication-title: J Pediatr doi: 10.1016/j.jpeds.2006.11.043 – volume: 131 start-page: 1262 year: 2000 ident: 2023041308192708500_ article-title: Differential vasoconstrictor activity of human urotensin-II in vascular tissue isolated from the rat, mouse, dog, pig, marmoset and cynomolgus monkey publication-title: Br J Pharmacol doi: 10.1038/sj.bjp.0703690 – volume: 26 start-page: 128 year: 2009 ident: 2023041308192708500_ article-title: Lack of association between obesity and left ventricular systolic dysfunction publication-title: Echocardiography doi: 10.1111/j.1540-8175.2008.00764.x – volume: 93 start-page: 246 year: 2003 ident: 2023041308192708500_ article-title: Direct actions of urotensin II on the heart: implications for cardiac fibrosis and hypertrophy publication-title: Circ Res doi: 10.1161/01.RES.0000084382.64418.BC – volume: 3 start-page: 239 year: 2013 ident: 2023041308192708500_ article-title: Role of urotensin II gene polymorphisms in susceptibility to the development of essential hypertension in a Northern Han Chinese population publication-title: J Cardiovasc Pulmon Dis – volume: 19 start-page: 2185 year: 2001 ident: 2023041308192708500_ article-title: Co-expression of urotensin II and its receptor (GPR14) in human cardiovascular and renal tissues publication-title: J Hypertens doi: 10.1097/00004872-200112000-00011 – volume: 31 start-page: 1326 year: 2010 ident: 2023041308192708500_ article-title: Urotensin II induction of adult cardiomyocytes hypertrophy involves the Akt/GSK-3beta signaling pathway publication-title: Peptides doi: 10.1016/j.peptides.2010.04.009 – volume: 370 start-page: 238 year: 2004 ident: 2023041308192708500_ article-title: Urotensin-II-mediated cardiomyocyte hypertrophy: effect of receptor antagonism and role of inflammatory mediators publication-title: Naunyn Schmiedebergs Arch Pharmacol doi: 10.1007/s00210-004-0980-z – volume: 10 start-page: 921 year: 2012 ident: 2023041308192708500_ article-title: Association between Thr21Met and Ser89Asn polymorphisms of the urotensin-II (UTS2) gene, diabetes mellitus, and diabetic retinopathy publication-title: Curr Eye Res doi: 10.3109/02713683.2012.688181 – volume: 92 start-page: 201 year: 2016 ident: 2023041308192708500_ article-title: Role of UTS2 gene in the genetic susceptibility to atrial fibrillation in the Chinese population publication-title: Postgrad Med J doi: 10.1136/postgradmedj-2015-133699 – volume: 76 start-page: 1186 year: 2009 ident: 2023041308192708500_ article-title: Urotensin II induces rat cardiomyocyte hypertrophy via the transient oxidization of Src homology 2-containing tyrosine phosphatase and transactivation of epidermal growth factor receptor publication-title: Mol Pharmacol doi: 10.1124/mol.109.058297 – volume: 115 start-page: 538 year: 2005 ident: 2023041308192708500_ article-title: Toward transcriptional therapies for the failing heart: chemical screens to modulate genes publication-title: J Clin Invest doi: 10.1172/JCI24144 – volume: 28 start-page: 36 year: 2007 ident: 2023041308192708500_ article-title: Urotensin II accelerates cardiac fibrosis and hypertrophy of rats induced by isoproterenol publication-title: Acta Pharmacol Sin doi: 10.1111/j.1745-7254.2007.00485.x – volume: 109 start-page: 1580 year: 2004 ident: 2023041308192708500_ article-title: Hypertrophy of the heart: a new therapeutic target? publication-title: Circulation doi: 10.1161/01.CIR.0000120390.68287.BB – volume: 102 start-page: 470 year: 2000 ident: 2023041308192708500_ article-title: Left ventricular hypertrophy: pathogenesis, detection, and prognosis publication-title: Circulation doi: 10.1161/01.CIR.102.4.470 – volume: 34 start-page: 272 year: 2006 ident: 2023041308192708500_ article-title: Association of ACE, ACE2 and UTS2 polymorphisms with essential hypertension in Han and Dongxiang populations from north-western China publication-title: J Int Med Res doi: 10.1177/147323000603400306 – volume: 27 start-page: 1659 year: 2006 ident: 2023041308192708500_ article-title: Haplotypes in the urotensin II gene and urotensin II receptor gene are associated with insulin resistance and impaired glucose tolerance publication-title: Peptides doi: 10.1016/j.peptides.2006.02.008 – volume: 27 start-page: 2919 year: 2006 ident: 2023041308192708500_ article-title: Urotensin-II receptor blockade with SB-611812 attenuates cardiac remodeling in experimental ischemic heart disease publication-title: Peptides doi: 10.1016/j.peptides.2006.06.011 – volume: 401 start-page: 282 year: 1999 ident: 2023041308192708500_ article-title: Human urotensin-II is a potent vasoconstrictor and agonist for the orphan receptor GPR14 publication-title: Nature doi: 10.1038/45809 – start-page: e83137 volume-title: PLoS ONE year: 2013 ident: 2023041308192708500_ article-title: Urotensin-II system in genetic control of blood pressure and renal function – volume: 56 start-page: 56 year: 1975 ident: 2023041308192708500_ article-title: Wall stress and patterns of hypertrophy in the human left ventricle publication-title: J Clin Invest doi: 10.1172/JCI108079 |
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| Snippet | ObjectiveCardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli, some of which might finally lead up to a maladaptive... Cardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli, some of which might finally lead up to a maladaptive state.... Objective Cardiac hypertrophy is the heart's response to a variety of extrinsic and intrinsic stimuli, some of which might finally lead up to a maladaptive... |
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| SubjectTerms | Adult Alleles Cardiology Cardiomegaly - genetics Cardiomyocytes Cardiomyopathy Case-Control Studies China Deoxyribonucleic acid Diabetes Diabetic retinopathy DNA Female Genes Genotype Heart Humans Hypertension Hypertension - genetics Linkage Disequilibrium Male Middle Aged Peptide Hormones - genetics Peptides Polymerase Chain Reaction Polymorphism, Restriction Fragment Length Polymorphism, Single Nucleotide Population Rodents Sex Factors Statistical analysis |
| Title | Genetic polymorphisms of UTS2 rs2890565 Ser89Asn in cardiac hypertrophy in Chinese Han population |
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