Dissecting the genetics of chronic mucus hypersecretion in smokers with and without COPD

Eur Respir J. 2015 Jan;45(1):60-75. doi: 10.1183/09031936.00093314. Epub 2014 Sep 18.

Abstract

Smoking is a notorious risk factor for chronic mucus hypersecretion (CMH). CMH frequently occurs in chronic obstructive pulmonary disease (COPD). The question arises whether the same single-nucleotide polymorphisms (SNPs) are related to CMH in smokers with and without COPD. We performed two genome-wide association studies of CMH under an additive genetic model in male heavy smokers (≥20 pack-years) with COPD (n=849, 39.9% CMH) and without COPD (n=1348, 25.4% CMH), followed by replication and meta-analysis in comparable populations, and assessment of the functional relevance of significantly associated SNPs. Genome-wide association analysis of CMH in COPD and non-COPD subjects yielded no genome-wide significance after replication. In COPD, our top SNP (rs10461985, p=5.43×10(-5)) was located in the GDNF-AS1 gene that is functionally associated with the GDNF gene. Expression of GDNF in bronchial biopsies of COPD patients was significantly associated with CMH (p=0.007). In non-COPD subjects, four SNPs had a p-value <10(-5) in the meta-analysis, including a SNP (rs4863687) in the MAML3 gene, the T-allele showing modest association with CMH (p=7.57×10(-6), OR 1.48) and with significantly increased MAML3 expression in lung tissue (p=2.59×10(-12)). Our data suggest the potential for differential genetic backgrounds of CMH in individuals with and without COPD.

Publication types

  • Meta-Analysis
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Alleles
  • Biopsy
  • Bronchi / pathology
  • Cohort Studies
  • Gene Expression Profiling
  • Genome-Wide Association Study
  • Glial Cell Line-Derived Neurotrophic Factor / genetics
  • Humans
  • Lung / metabolism
  • Mucus / metabolism*
  • Polymorphism, Single Nucleotide
  • Pulmonary Disease, Chronic Obstructive / genetics*
  • Pulmonary Disease, Chronic Obstructive / metabolism*
  • Quantitative Trait Loci
  • RNA, Messenger / metabolism
  • Risk Factors
  • Smoking / adverse effects*

Substances

  • GDNF protein, human
  • Glial Cell Line-Derived Neurotrophic Factor
  • RNA, Messenger

Grants and funding