Objective
To detect the plasma contents of cyclin-dependent kinase 5 (CDK5) and phosphorylated-peroxisome proliferators-activated receptors γ (P-PPARγ) in pulmonary hypertension (PH) secondary to chronic obstructive pulmonary disease (COPD) and explore the clinical significance.
Methods
A total of 60 COPD patients with PH and 20 COPD patients without PH were enrolled in this study, with 20 volunteers with normal pulmonary function as controls.These subjects were divided into control and COPD groups, and mild, moderate and severe PH groups.Pulmonary artery systolic pressure (PASP) was determined by Doppler echocardiograph and the severity (mild, moderate and severe) of PH secondary to COPD was evaluated.The plasma contents of CDK5 and P-PPARγ were determined using ELISA kits.Correlation between the two plasma markers and PASP was analyzed using Pearson′s correlation.ROC curve was drawn to assess the diagnostic accuracy of the two plasma markers in PH.
Results
The plasma contents of CDK5 and P-PPARγ in COPD patients with PH were higher than those in the control subjects and COPD patients without PH respectively.The plasma contents of the two markers were the highest in the severe PH group, lower in the moderate PH group.Positive correlation were found between the plasma markers and PASP (r=0.789, P=0.000; r=0.649, P=0.000), and between plasma CDK5 and plasma P-PPARγ (r=0.674, P=0.000). Area under ROC curve of diagnosing PH using CDK5 and P-PPARγ were 0.762 and 0.836 respectively.Plasma content of CDK5>115.91 ng/L was found to be 60.0% sensitive and 87.5% specific for diagnosing PH, and plasma content of P-PPARγ>95.34 ng/L was found to be 80.0% sensitive and 75.0% specific for diagnosing PH.
Conclusions
Upregulation of plasma CDK5 and phosphorylation of PPARγ could be important pathologic changes in PH secondary to COPD.The plasma contents of CDK5 and P-PPARγ can help to identify PH and assess the PH severity in clinic.
Key words:
Chronic obstructive pulmonary disease; Pulmonary hypertension; Cyclin-dependent kinase 5; Phosphorylation of PPARγ