Association Study of Common Variants in PFN1 With Hypertension in a Han Chinese Population: A Case–Control Study and A Follow-up Study

Autor: Yanchun Chen, Chong Shen, Xianghai Zhao, Pengfei Wei, Hailong Zhao, Junxiang Sun, Qian Zhuang, Chunlan Liu, Song Yang, Xiaotian Chen
Rok vydání: 2017
Předmět:
Male
0301 basic medicine
Blood Pressure
030204 cardiovascular system & hematology
Profilins
0302 clinical medicine
Risk Factors
Odds Ratio
education.field_of_study
Incidence
Confounding
Middle Aged
Phenotype
Hypertension
Cardiology
Female
China
medicine.medical_specialty
Population
Single-nucleotide polymorphism
Polymorphism
Single Nucleotide

03 medical and health sciences
Asian People
Internal medicine
Internal Medicine
medicine
Humans
Genetic Predisposition to Disease
education
Antihypertensive Agents
Genetic Association Studies
Aged
Proportional Hazards Models
Genetic association
Chi-Square Distribution
business.industry
Haplotype
Case-control study
medicine.disease
Logistic Models
030104 developmental biology
Blood pressure
Endocrinology
Haplotypes
Case-Control Studies
Phosphopyruvate Hydratase
Linear Models
Arterial stiffness
business
Follow-Up Studies
Zdroj: American Journal of Hypertension. 30:1024-1031
ISSN: 1941-7225
0895-7061
Popis: BACKGROUND Animal researches reported that the dysfunction of profilin1 (PFN1) was involved in the physiological arterial stiffness and vascular remodeling linking to the etiology of hypertension (HT). This study mainly aims at evaluating the association of PFN1 and HT in a Han Chinese population. METHODS A case-control study consisted of 2,012 HT cases and 2,210 controls was conducted and 2,116 participants from the healthy controls were further followed up for average 5.01 years. Logistic and Cox regression models were applied to evaluate the association of 4 tag single nucleotide polymorphisms (SNPs) of PFN1 and ENO3 with HT. RESULTS There was no significant association of the 4 SNPs between HT cases and controls even after adjustment for confounding factors (P > 0.05). Haplotype analysis did not identify any significant haplotype with HT. There were no statistical difference of systolic blood pressure (BP) and diastolic BP among different genotypes in antihypertensive-treated group and untreated group. In follow-up population, there was no significant association of candidate SNPs with HT even after adjustment for covariates (all P > 0.05). Of note, the plasma profilin1 level of HT cases was significantly higher than that of control subjects (P = 0.011). The profilin1 levels of controls significantly decreased with variation of rs238243 at PFN1 (P = 0.041), and the profilin1 levels of HT cases increased with variation of rs238238 at ENO3 (P = 0.004). CONCLUSIONS Our results suggest that HT cases displayed an elevated plasma profilin1. Variants of rs238243 and rs238238 might regulate profilin1 expression by epigenetic modification and indirectly affects the susceptible threshold of HT.
Databáze: OpenAIRE