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Original article
DOI: 10.1016/j.arbres.2018.07.021
Association of HTR2A-1438G/A Genetic Polymorphism With Smoking and Chronic Obstructive Pulmonary Disease
Asociación del polimorfismo genético HTR2A-1438G/A con el tabaco y la enfermedad pulmonar obstructiva crónica
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Zoraida Verdea,
Corresponding author
zoraida.verde@uva.es

Corresponding author.
, Catalina Santiagob, Luis M. Chicharroc, Fernando Bandrésd, Félix Gómez-Gallegoe, Jose Miguel Rodríguez González-Morof, Pilar de Lucasg
a Department of Biochemistry, Molecular Biology and Physiology, Universidad de Valladolid, Soria, Spain
b Department of Biomedical Sciences, Universidad Europea, Villaviciosa de Odón, Madrid, Spain
c Cátedra Complutense Diagnostic and Innovation, Universidad Complutense, Madrid, Spain
d Department of Toxicology and Health Sanitary, Universidad Complutense, Madrid, Spain
e School of Health Sciences, Universidad Internacional de La Rioja, Madrid, Spain
f Department of Neumology, Hospital Universitario Príncipe de Asturias, Alcalá de Henares, Madrid, Spain
g Department of Neumology, Hospital General Universitario Gregorio Marañón, Madrid, Spain
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Received 14 May 2018, Accepted 26 July 2018
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Tables (3)
Table 1. Patients and healthy controls characteristics.
Table 2. Genotypes between smokers groups.
Table 3. The association between genotypes, phenotypes and smoking habits.
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Figures (1)
Abstract
Introduction

Cigarette smoking is a major risk factor in the development of chronic obstructive pulmonary disease (COPD). Serotonin levels have been associated with COPD and smoking has been as a significant modulator. Elevated levels of serotonin are responsible for bronchoconstriction and pulmonary vasoconstriction and also nicotine dependence, thus serotonin response could be affected by genetic polymorphisms in transporters and receptors of serotonin.

Objectives

The aim of the current study was to analyze the effect of SLC6A4 (5HTT_LPR) (rs25531) and HTR2A-1438G/A (rs6311) genetic polymorphisms on the relation between smoking habits and COPD.

Methods

The association between SLC6A4 (5HTT_LPR) (rs25531), HTR2A-1438G/A (rs6311), smoking degree and COPD was analyzed in a total of 77 COPD patients (active smokers) and 90 control subjects (active healthy smokers). The DNA was extracted of peripheral leukocytes samples and genotyping was performed using an allele specific polymerase chain reaction.

Results

The distribution of SLC6A4 genotypes did not vary between healthy smokers and COPD patients (P=0.758). On the other hand, the A allele of HTR2A (rs6311) was significantly associated with COPD incidence in the trend model (P=0.02; 1.80 [1.04–3.11]). Among all smokers, this allele was also associated with the number of pack years smoked (P=0.02) and also, we observed a marginal association with FEV1/FVC values (P=0.06).

Conclusion

Our results point a possible role of the A allele of HTR2A (rs6311) in COPD pathogenesis, suggesting that this effect depends partly on tobacco consumption due to a gene-by-environment interaction.

Keywords:
Serotonin
HTR2A
SLC6A4
Smoking
Chronic obstructive pulmonary disease
Genetic polymorphisms
Abbreviations:
BMI
COPD
PH
ERS
FEV1
FVC
MAO
Serotonin
SLC6A4
STREGA
TPH2
HTR2A
5-HTT
Resumen
Introducción

El consumo de tabaco es el principal riesgo para desarrollar enfermedad pulmonar obstructiva crónica (EPOC). Los niveles de serotonina se han relacionado con el riesgo de desarrollo de EPOC, siendo el consumo de tabaco un modulador significativo.

Los niveles elevados de serotonina producen broncoconstricción y vasoconstricción pulmonar, así como dependencia a la nicotina. Así, la respuesta a serotonina podría verse afectada por los polimorfismos genéticos en los transportadores y receptores de este neurotransmisor.

Objetivos

El objetivo de este estudio fue analizar el papel de los polimorfismos genéticos SLC6A4 (5HTT_LPR) (rs25531) y HTR2A -1438G/A (rs6311) en la relación entre el consumo de tabaco y la EPOC.

Métodos

Se analizó la asociación entre SLC6A4 (5HTT_LPR) (rs25531), HTR2A -1438G/A (rs6311), grado de tabaquismo y EPOC en 77 pacientes con EPOC (fumadores activos) y 90 sujetos control (fumadores activos sanos). El ADN se extrajo a partir de leucocitos de sangre periférica y la genotipificación se realizó utilizando la reacción en cadena de la polimerasa alelo-específica.

Resultados

No se observaron diferencias en la distribución de genotipos SLC6A4 entre fumadores sanos y fumadores con EPOC (p=0,758). Se encontró una asociación significativa entre el alelo A de HTR2A (rs6311) y la incidencia de EPOC en el modelo predictivo (p=0,02; 1,80 [1,04-3,11]). En los fumadores, este alelo también se asoció al número de paquetes fumados al año (p=0,02) y, además, de forma marginal con los valores de FEV1/FVC (p=0,06).

Conclusión

Nuestros resultados apuntan a un posible papel del alelo A de HTR2A (rs6311) en la patogénesis de EPOC, indicando que este efecto dependería en parte del consumo de tabaco a través de una interacción gen-ambiente.

Palabras clave:
Serotonina
HTR2A
SLC6A4
Consumo de tabaco
Enfermedad pulmonar obstructiva crónica
Polimorfismos genéticos
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