Association of ADAM33 gene polymorphism and arginase activity with susceptibility to ventilatory impairment in wood dust-exposed workers

Abstract

<jats:p> ADAM33 represents an important gene of susceptibility for lung function impairment. This work aimed to evaluate the association between genetic polymorphism of ADAM33 at four single nucleotide polymorphisms (T1, T2, S1, and Q1) and arginase activity with respiratory functions impairment in wood workers. The study was done to compare ventilatory functions and arginase activity of 82 wood workers and 81 controls. Genotyping was determined by using the polymerase chain restriction fragment length polymorphism method. Forced expiratory volume in the first second (FEV<jats:sub>1</jats:sub>), forced vital capacity (FVC), and peak expiratory flow rate (PEF) of the workers were significantly reduced compared with the controls. T1 single nucleotide polymorphism (SNP) was associated with obvious decline in the FEV<jats:sub>1</jats:sub>, FVC, and PEF in wood workers, while T2 SNP was associated with decline in FEV<jats:sub>1</jats:sub> and PEF. A significant increase in arginase activity was found in T2 and S1 SNPs of the exposed workers. Increase in duration of exposure was correlated with the decline in ventilatory functions. This inverse correlation was significant for pulmonary function indices in AA and GG genotypes of T1 and T2, respectively. Moreover, significance was detected for FVC and FEV<jats:sub>1</jats:sub> in AA and GA genotypes of S1 and Q1. A positive correlation between arginase activity and duration of exposure was found to be significant in GG genotype of S1 SNP. An association between ADAM33 gene polymorphism and impaired lung functions was detected in wood dust-exposed workers. Arginase activity may play an associated important role in increasing this impairment in wood workers. </jats:p>

Silencing of ADAM33 restrains proliferation and induces apoptosis of airway smooth muscle cells in ovalbumin‐induced asthma model

“…ADAM proteins were reported to play a vital role in cell fusion, cell signaling, cell adhesion, and proteolysis . ADAM33 was identified as an important asthma susceptibility gene for lung function impairment; however, how ADAM33 causes and promotes asthma remains to be further investigated . Further, ADAM33 was mainly expressed in ASMCs and indicated to regulate the function of ASMCs .…”

“…11 ADAM33 was identified as an important asthma susceptibility gene for lung function impairment; however, how ADAM33 causes and promotes asthma remains to be further investigated. 12,13 Further, ADAM33 was mainly expressed in ASMCs and indicated to regulate the function of ASMCs. 14 At present, many research referring to the effects of ADAM33 T1, S2, V4, and T + 1 polymorphisms on asthma and chronic obstructive pulmonary disease have been published.…”

Response to Baur et al. (2017)

“…Even after controlling for confounders such as age, smoking history, job task etc, there may be a wide variety of lung function impairment. This is probably influenced by genetic factors as has been shown in numerous studies, including on twins, genetic polymorphisms, and pharmacokinetics …”