Association Between the Angiotensin-Converting Enzyme Gene Polymorphisms and Tissue Oxygenation During Exercise in Patients With COPD

Kanazawa, Hiroshi; Otsuka, Toshihiro; Hirata, Kazuto; Yoshikawa, Junichi

doi:10.1378/chest.121.3.697

Cited by 49 publications

(29 citation statements)

References 11 publications

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“…ACE polymorphic variation has been identified in association with different clinical features of COPD, such as a disturbance in peripheral tissue oxygenation during exercise (Kanazawa et al, 2002), the regulation of skeletal muscle aerobic work efficiency (Zhang et al, 2008), the severity of skeletal muscle weakness (Hopkinson et al, 2004), and pulmonary hypertension evoked by exercise challenge (Kanazawa et al, 2000). Several molecular epidemiological studies have been conducted to evaluate the risk of COPD association with the I/D polymorphism of the ACE gene.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of whether the ACE gene I/D polymorphism constitutes a risk factor for chronic obstructive pulmonary disease in the Turkish population

Ayada¹,

Toru²,

Genç³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow obstruction that occurs as a result of the normal inflammatory process to protect against harmful irritants and chemicals. Another physiological regulatory process, the renin angiotensin system (RAS), plays an important role in the pathology of many diseases. Angiotensin converting enzyme (ACE) is a key enzyme of RAS. We investigated the frequency of the ACE gene I/D polymorphism in patients with COPD in Turkey. This study was performed on 47 unrelated patients with COPD and 64 healthy subjects. DNA samples were isolated from peripheral blood, and ACE DNA was amplified by polymerase chain reaction. The frequencies of ACE genotypes were 27.7, 55.3, and 17% for DD, ID, and II in the COPD group, respectively, and 43.8, 43.8, and 12.4% in the control group. There was no statistically significant difference between groups (c 2 = 3.078; df = 2; P = 0.220). The distributions of ACE gene D alleles were 38.2% (N = 52) in the COPD group and 61.8% (N = 84) in the control group; and those of I alleles were 48.8% (N = 42) in the COPD group and 51.2% (N = 44) in the control group. There was no statistically significant difference between groups for allele frequency (c 2 = 2.419; df = 2; P = 0.120). We believe these results can be useful for large-scale population genetic research considering the frequency of the ACE gene variation in COPD patients in the Turkish population.

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Section: Discussionmentioning

confidence: 99%

Evaluation of whether the ACE gene I/D polymorphism constitutes a risk factor for chronic obstructive pulmonary disease in the Turkish population

Ayada¹,

Toru²,

Genç³

et al. 2014

Genet. Mol. Res.

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“…Busquets et al (2007) showed that the DD genotype was associated with an increased risk of a smoker developing COPD and, unexpectedly, that the ID genotype is more prevalent in individuals that smoke. Kanazawa et al (2002) investigated the association between ACE polymorphisms and tissue oxygenation during exercise in patients with COPD and concluded that the ACE DD genotype might be associated with a disturbance in peripheral tissue oxygenation during exercise in patients with COPD. Zhang et al (2008) reported an association between the ACE gene polymorphism and exercise ventilatory response and skeletal muscle aerobic work efficiency in COPD patients.…”

Section: Discussionmentioning

confidence: 99%

“…Under some conditions, the ACE D allele amplified more effectively than the longer I allele, resulting in mistyping of the ID genotype as DD (Ueda et al, 1996;Kanazawa et al, 2002). To address this, the sense primer used in the PCR was replaced with an insertionspecific primer that lead to the selective amplification of the I allele, which could now be detected in previously mistyped ID genotypes.…”

Section: Genotypingmentioning

confidence: 99%

The insertion/deletion polymorphism in the ACE gene and chronic obstructive pulmonary disease

Şimşek

Tekeş²,

Oral³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. An insertion/deletion (I/D) polymorphism was identified in intron 16 of the gene encoding the human angiotensin I-converting enzyme (ACE), a candidate gene for chronic obstructive pulmonary disease (COPD). We investigated the relationship between this polymorphism in the ACE gene and the risk of developing COPD. Sixty-six COPD in-patients and 40 non-smoking control individuals were recruited for this study. The distribution of ACE genotypes in these individuals was studied. The frequencies of ACE genotypes were found to be 47.0% for DD, 30.3% for ID, and 22.7% for II in the COPD group and 32.5% for DD, 47.5% for ID, and 20.0% for II in the control group. The allele frequencies were found to be 0.62% for the D allele and 0.38% for the I allele in the COPD group and 0.56% for the D allele and 0.44% for the I allele in the control group. A significant difference ACE gene and chronic obstructive pulmonary disease was found between I and D allele frequencies (P < 0.05) of the study and control groups. Our results suggest that this ACE polymorphism may be associated with the development of COPD.

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“…The vast majority of the total activity of ACE in the body is found in lung tissue and increases further after stimulation by chronic hypoxia (Kanazawa et al 2002). An insertion/deletion (I/D) polymorphism at intron 16 of the ACE gene has been associated with increased risk of systemic arterial hypertension (O'Donnell et al 1998), atherosclerosis (Tkac et al 2003) and also with resting pulmonary artery pressure in Caucasian patients with COPD (Tkacova et al 2005).…”

Section: Serotonin Transportermentioning

confidence: 99%

The role of gene polymorphisms in the pathogenesis of chronic obstructive pulmonary disease

et al. 2008

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Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Irreversible airflow limitation, both progressive and associated with an inflammatory response of the lungs to noxious particles or gases, is a hallmark of the disease. Cigarette smoking is the most important environmental risk factor for COPD, nevertheless, only approximately 20-30% of smokers develop symptomatic disease. Epidemiological studies, case-control studies in relatives of patients with COPD, and twin studies suggest that COPD is a genetically complex disease with environmental factors and many involved genes interacting together. Two major strategies have been employed to identify the genes and the polymorphisms that likely contribute to the development of complex diseases: association studies and linkage analyses. Biologically plausible pathogenetic mechanisms are prerequisites to focus the search for genes of known function in association studies. Protease-antiprotease imbalance, generation of oxidative stress, and chronic inflammation are recognized as the principal mechanisms leading to irreversible airflow obstruction and parenchymal destruction in the lung. Therefore, genes which have been implicated in the pathogenesis of COPD are involved in antiproteolysis, antioxidant barrier and metabolism of xenobiotic substances, inflammatory response to cigarette smoke, airway hyperresponsiveness, and pulmonary vascular remodelling. Significant associations with COPD-related phenotypes have been reported for polymorphisms in genes coding for matrix metalloproteinases, microsomal epoxide hydrolase, glutathione-S-transferases, heme oxygenase, tumor necrosis factor, interleukines 1, 8, and 13, vitamin D-binding protein and β-2-adrenergic receptor (ADRB2), whereas adequately powered replication studies failed to confirm most of the previously observed associations. Genome-wide linkage analyses provide us with a novel tool to identify the general locations of COPD susceptibility genes, and should be followed by association analyses of positional candidate genes from COPD pathophysiology, positional candidate genes selected from gene expression studies, or dense single nucleotide polymorphism panels across regions of linkage. Haplotype analyses of genes with multiple polymorphic sites in linkage disequilibrium, such as the ADRB2 gene, provide another promising field that has yet to be explored in patients with COPD. In the present article we review the current knowledge about gene polymorphisms that have been recently linked to the risk of developing COPD and/or may account for variations in the disease course.

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Association Between the Angiotensin-Converting Enzyme Gene Polymorphisms and Tissue Oxygenation During Exercise in Patients With COPD

Cited by 49 publications

References 11 publications

Evaluation of whether the ACE gene I/D polymorphism constitutes a risk factor for chronic obstructive pulmonary disease in the Turkish population

Evaluation of whether the ACE gene I/D polymorphism constitutes a risk factor for chronic obstructive pulmonary disease in the Turkish population

The insertion/deletion polymorphism in the ACE gene and chronic obstructive pulmonary disease

The role of gene polymorphisms in the pathogenesis of chronic obstructive pulmonary disease

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