Literature DB >> 29804144

SERPINA1 Hepatocyte-Specific Promoter Polymorphism Associate with Chronic Obstructive Pulmonary Disease in a Study of Kashmiri Ancestry Individuals.

Arif Bashir1, Younis M Hazari2, Samirul Bashir1, Nazia Hilal1, Mariam Banday1, Mir Khurshid Iqbal1, Tariq Rashid Jan3, Syed Suraiya Farooq4, Naveed Nazir Shah5, Khalid Majid Fazili6.   

Abstract

PURPOSE: Different mutations in coding and non-coding sequences of the SERPINA1 gene have been implicated in the pathogenesis of COPD. However, - 10T/C mutation in the hepatocyte-directed promoter region has not been associated with COPD pathogenesis so far. Here, we report an increased frequency of - 10C genotype that is associated with decreased levels of serum alpha1-antitrypsin (α1AT) in COPD patients.
METHODS: The quantification of serum α1AT was done by ELISA, the phenol-chloroform method was used for DNA extraction, PCR products were directly sequenced. The IBM SPSS Statistics v21 software was used for statistical analyses of the data.
RESULTS: The mean serum α1AT level was found to be 1.203+0.239 and 3.162+0.160 g/L in COPD cases and in control, respectively. The - 10C allele is associated with an increased risk of COPD [OR, 3.50 (95%CI, 1.86-6.58); p < 0.001]. The combined variant genotype (TT+CC) was significantly found associated with an increased risk of COPD [OR, 3.20 (95% CI, 1.47-6.96); p = 0.003]. A significant association of the family history with COPD (overall p value= 0.0331) suggests that genetics may play an important role in the pathogenesis of COPD.
CONCLUSION: The polymorphism associated with hepatocyte-specific promoter region (- 10T/C) is likely to be associated with the pathogenesis of COPD. It is quite possible that the change of the base in the hepatocyte-specific promoter of the SERPINA1 gene can modulate its strength, thereby driving the reduced expression of α1AT.

Entities:  

Keywords:  COPD: Chronic obstructive pulmonary disease; SERPIN1A: Serine protease inhibitor 1A; α1AT: Alpha1-antitrypsin

Mesh:

Substances:

Year:  2018        PMID: 29804144     DOI: 10.1007/s00408-018-0124-8

Source DB:  PubMed          Journal:  Lung        ISSN: 0341-2040            Impact factor:   2.584


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