Association of SCNN1B promoter methylation with essential hypertension.
Mol Med Rep
; 14(6): 5422-5428, 2016 Dec.
Article
em En
| MEDLINE
| ID: mdl-27840946
ABSTRACT
The amiloride-sensitive sodium channel beta subunit (SCNN1B) gene encodes the beta subunit of the epithelial sodium channel, which is involved in blood pressure homeostasis. The aim of the present study was to investigate the association between SCNN1B gene promoter methylation and essential hypertension (EH), and to explore whether SCNN1B methylation was altered by antihypertensive therapy. The present study recruited 282 individuals 94 controls, 94 incident cases and 94 prevalent cases. Subsequently, the methylation status of six CpG sites in the SCNN1B promoter region was measured using bisulfite pyrosequencing technology. Among the six CpG sites, a significant difference in CpG1 and CpG2 methylation levels were detected between controls and incident cases (CpG1 ßstandardized=0.17, adjusted P=0.015; CpG2 ßstandardized=0.41, adjusted P=0.001). In addition, a significant difference was detected in CpG1 methylation levels between incident cases and prevalent cases (ßstandardized=0.252, adjusted P=3.77E04). The present study also demonstrated that CpG1 and CpG2 methylation levels were significantly lower in males compared with in females (CpG1 t=3.180, P=0.002; CpG2 t=2.148, P=0.033). CpG1 methylation was also shown to be positively correlated with age (controls r=0.285, P=0.008; incident cases r=0.401, P=0.0001; prevalent cases r=0.367, P=0.001). These results indicated a significant association between EH and SCNN1B methylation, which was affected by age, gender and antihypertensive therapy.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Regiões Promotoras Genéticas
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Metilação de DNA
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Predisposição Genética para Doença
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Canais Epiteliais de Sódio
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Estudos de Associação Genética
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Hipertensão
Tipo de estudo:
Etiology_studies
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Prognostic_studies
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Risk_factors_studies
Limite:
Female
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Humans
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Male
Idioma:
En
Ano de publicação:
2016
Tipo de documento:
Article