Paraoxonase-1 Is Associated With Corneal Endothelial Cell Alterations in Patients With Chronic Obstructive Pulmonary Disease

2013 ◽  
Vol 54 (8) ◽  
pp. 5852 ◽  
Author(s):  
Núria Soler ◽  
Anabel García-Heredia ◽  
Judit Marsillach ◽  
Bharti Mackness ◽  
Michael Mackness ◽  
...  
Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1891
Author(s):  
Jun Watanabe ◽  
Kazuhiko Kotani ◽  
Alejandro Gugliucci

Oxidative stress is a driving factor in the pathophysiology of chronic obstructive pulmonary disease (COPD). While paraoxonase 1 (PON1) is an antioxidant enzyme and a potential biomarker of this disease, data regarding the status of PON-1 in COPD are inconclusive. In this regard, to shed light on this issue, we performed a meta-analysis of data on PON1 activity in COPD. Electronic databases (MEDLINE, Embase and CENTRAL) were searched for available studies on PON1 activity in patients with stable COPD published before October 2021. A meta-analysis was performed using random-effects models. Twelve studies (12 studies on paraoxonase and three on arylesterase) were identified. Patients with COPD had lower levels of paraoxonase activity (standard mean difference [SMD] −0.77, 95% confidence interval [CI] −1.35 to −0.18) and arylesterase activity (SMD −1.15, 95% CI −1.95 to −0.36) in comparison to healthy controls. In subgroup analyses, paraoxonase activity was lower in patients of studies as consisted of mainly non-severe COPD (SMD −1.42, 95% CI −2.04 to −0.79) and, by contrast, slightly higher in patients of studies including severe COPD (SMD 0.33, 95% CI 0.02 to 0.64) in comparison to healthy controls. Arylesterase activity showed a similar trend. Overall, PON1 activity was lower in patients with COPD, suggesting that PON1-related antioxidant defense is impaired in COPD. Future studies are warranted.


2018 ◽  
Vol 71 (11) ◽  
pp. 963-970
Author(s):  
Marija Grdić Rajković ◽  
Sanja Popović-Grle ◽  
Andrea Vukić Dugac ◽  
Dunja Rogić ◽  
Ivana Rako ◽  
...  

AimsChronic obstructive pulmonary disease (COPD) is characterised with oxidative stress. Paraoxonase 1 (PON1) is an enzyme, coded by PON1 gene, with distinctive antiatherogenic and antioxidative roles. We aimed to investigate the frequencies of Q192R, L55M and −108C>T polymorphisms and association of those polymorphisms with paraoxonase and arylesterase activities in patients with COPD.MethodsPON1 genotype was determined by PCR–restriction fragment length polymorphism method. PON1 activity was measured by paraoxon and phenylacetate.ResultsOnly −108C>T polymorphism resulted in significantly different distribution of genotypes and alleles, with higher frequency of TT genotype and T allele in patients compared with control subjects. Moreover, T allele (OR 2.29 (95% CI 1.54 to 3.41); p<0.001) as well as TT genotype (OR 5.00 (95% CI 2.19 to 11.43); p<0.001) showed an association with the disease. −108C>T polymorphism was suggested as a significant diagnostic predictor for the disease (OR (95% CI) 2.65 (1.53 to 4.59), p=0.001), with an area under the receiver operating characteristic curve of 0.90 (95% CI 0.84 to 0.93) and with 83.90% of correctly classified cases.ConclusionsHigher frequency of TT genotype and T allele could contribute to the observed reduction of PON1 activity in patients with COPD. T allele and TT genotype are associated with COPD, and the PON1−108C>T polymorphism could be a potential predictor of the disease.


2014 ◽  
Vol 11 (5) ◽  
pp. 539-545 ◽  
Author(s):  
Lada Rumora ◽  
Marija Grdić Rajković ◽  
Lara Milevoj Kopčinović ◽  
Dolores Pancirov ◽  
Ivana Čepelak ◽  
...  

2001 ◽  
Vol 7 (3) ◽  
pp. 205-208 ◽  
Author(s):  
Giuseppe Cella ◽  
Alessandra Sbarai ◽  
Gabriella Mazzaro ◽  
Barbara Vanzo ◽  
Silvia Romano ◽  
...  

We studied some endothelial cell activity plasma markers, nitric oxide (NO), thrombomodulin (TM), selectins (sP-, sE-,sL-selectin:platelet-P, endothelium-E, leukocyte-L), and tissue factor pathway inhibitor (TFPI) in 14 patients with chronic obstructive pulmonary disease (COPD), matched with 20 normal controls, to evaluate their endothelial cell dysfunction. Both NO (patients: 23.42 ± 1.67 μg/mL; controls: 40.0 ± 3.38 μg/mL) and TM levels (patients: 5.46 ± 1.32 ng/mL; controls : 12.9 ± 0.51 ng/mL) were significantly decreased in COPD (p < 0.001). sP-selectin levels (patients: 79.42 ± 18.20 ng/mL, controls: 37.5 ± 2.84 mg/mL) were significantly higher (p < 0.02), whereas sL-selectin levels (patients: 584.9 ± 78.98 ng/mL, controls: 1054.02 ± 61.28 ng/mL) were significantly decreased in patients with COPD (p < 0.001). In contrast, no differences were seen in sE-selectin. Patients with COPD showed a significantly higher (p < 0.001) TFPI antigen plasma level (mean 112.28 ± 6.45 ng/mL; controls 77.68 ± 0.28 ng/mL) than controls. Our data support the concept of some form of endothelial cell dysfunction, and coagulation abnormalities are present in patients with COPD. However, because the endothelium seems to produce a defense mechanism, the potential usefulness of an antithrombotic therapy in these patients needs further investigation.


2018 ◽  
Vol 47 (5) ◽  
pp. 1809-1818 ◽  
Author(s):  
Min Lv ◽  
Dajun Sun ◽  
Libo Chen

Background/Aims: In the treatment of serious and symptomatic coronary heart disease (CHD), coronary artery bypass grafting (CABG) is a frequently utilized intervention. In addition, the risk of CHD is strongly associated with the low activity of paraoxonase-1 (PON1), whose 3’-UTR harbors an rs3735590 polymorphism. The aim of this study was to investigate whether the rs3735590 polymorphism could be used as a prognosis marker in chronic obstructive pulmonary disease (COPD) patients undergoing CABG. In addition, the hypothesis, i.e., the rs3735590 polymorphism may be involved in the regulation of PON1 gene expression via modulating its interaction with miRNAs, was tested in this study. Methods: 292 patients diagnosed with COPD and treated with CABG were recruited for this study. Genomic DNA was extracted from clinical samples, and real-time quantitative PCR and Western-blot were used to measure the expression of miR-616 and PON1 in liver cells of different genotypes. Results: 292 COPD patients were divided into three groups according to their genotypes, i.e., rs3735590: CC (212), TC (75), and TT (5), respectively (TC and TT were merged in one group of T carriers for statistical analyses). Patients with the CC genotype were associated with a shorter event-free survival time as compared to patients with the T genotypes. In addition, PON1 was confirmed as a direct target gene of miR-616, while experiments with primary cells of different genotypes showed that miR-616 inhibited the expression of PON1 in CC cells. On the contrary, rs3735590 impaired such inhibitory effect of miR-616 in TT cells. Conclusion: The rs3735590 polymorphism of PON1 acts as a prognostic biomarker in COPD patients treated by CABG.


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