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.
lncRNA TUG1 regulates human pulmonary microvascular endothelial cell apoptosis via sponging of the miR‑9a‑5p/BCL2L11 axis in chronic obstructive pulmonary disease
