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Ye X.-W.,State Key Laboratory of Biotherapy of China | Ye X.-W.,University of Sichuan | Ye X.-W.,The Peoples Hospital of Guizhou Province | Xiao M.,State Key Laboratory of Biotherapy of China | And 9 more authors.
International Journal of Immunogenetics | Year: 2011

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease characterized by airway obstruction that is not fully reversible, and there is evidence of a hereditary component in COPD. We aimed to determine whether the polymorphisms -2548G/A of leptin (LEP) gene were associated with COPD and its severity in Chinese. A total of 456 subjects with COPD and 422 healthy controls from West China Hospital were enrolled in this study. COPD patients had been undergone a spirometry and a physical examination to refer the GOLD I-IV stages. The polymorphisms in the leptin promoter region at position -2548 G/A were detected by Polymerase chain reaction-restriction fragment length polymorphism analysis. The genotypes and alleles were scored, and the frequencies of the alleles and genotypes in patients and controls were compared. A significantly higher risk for COPD was observed for carriers of the LEP -2548 AA genotype [odds ratio (OR) = 7.87, 95% confidence interval (CI) 4.19-14.77, P < 0.001] and carriers of the LEP -2548 GA genotype (OR = 2.98, 95% CI 1.57-5.66, P = 0.001). The LEP -2548 A allele: frequency was significantly higher in the patient group compared with the control group (OR = 2.75, 95% CI: 2.20-3.44, P < 0.001). We also found a significant relationship between leptin gene polymorphism and the severity of COPD. In the present case-control study, we found an association between the -2548 G/A variant of the leptin gene and pathogenesis, severity of COPD in the Chinese population. It suggests that leptin -2548 G/A should be used as a genetic marker of COPD severity. © 2010 Blackwell Publishing Ltd.


Wu Y.-Q.,University of Sichuan | Wu Y.-Q.,State Key Laboratory of Biotherapy of China | Shen Y.-C.,University of Sichuan | Shen Y.-C.,State Key Laboratory of Biotherapy of China | And 15 more authors.
European Review for Medical and Pharmacological Sciences | Year: 2016

OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is both a pulmonary and systematic disease, which will cause abnormal expression of some circulating factors. Angiopoietin-like protein 4 (ANGPTL4) has been reported to play important role in inflammatory responses and several diseases. However, whether it contributes to COPD is an open question. The aim of this study is to explore the potent ial relat ionship between ANGPTL4 and COPD. PATIENTS AND METHODS: In this study, circulating levels of ANGPTL4, C-reactive protein (CRP), adiponectin, tumor necrosis factor (TNF)- α, matrix metalloproteinase (MMP)-9 and monocyte chemotactic protein (MCP)-1 in 73 COPD patients and 40 healthy volunteers were investigated using mul t iplex enzyme- l inked immunosorbent assay Kits. Then, we analyzed the correlations between ANGPTL4 with other inflammatory mediators and pulmonary function. RESULTS: Serum ANGPTL4 levels were significantly elevated in COPD patients compared with healthy controls (122.86 ± 38.59 ng/mL versus 99.03 ± 31.84 ng/mL, p = 0.001). Besides, serum ANGTPL4 levels were much higher in ever-smokers with COPD than in never-smokers with COPD (131.71 ± 32.92 ng/mL versus 113.25 ± 42.34 ng/mL, p = 0.03). More importantly, the concentrations of circulating ANGPLT4 correlated inversely with forced expiratory volume in 1 second (FEV1) % predicted, an index of lung function in COPD (r = -0.450, p < 0.001) and in all participants (r = -0.369, p < 0.001), while correlated positively with CRP (r = 0.312, p = 0.007 for COPD; r = 0.404, p < 0.001 for total subjects), adiponectin (r = 0.266, p = 0.004 for total subjects), and MMP-9 (r = 0.254, p = 0.03 for COPD). CONCLUSIONS: Our results suggest that circulating ANGPTL4 levels are up-regulated in COPD patients, and have correlations with pulmonary function and systematic inflammation in COPD, which provides a novel idea to further dig the pathogenic mechanisms of COPD, and just i f ies more studies to determine how ANGPTL4 contributes to COPD.

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