Reduced Apela/APJ system expression in patients with pulmonary artery hypertension secondary to chronic obstructive pulmonary disease

Background: Pulmonary artery hypertension (PAH) is a common disease that seriously threatens human physical and mental health. Chronic obstructive pulmonary disease (COPD) is the main cause of secondary PAH. Objectives: This study observed the differential expression of the endogenous Apela/APJ system in COPD patients with or without PAH. Methods: A total of 69 COPD patients were enrolled, including 31 patients with PAH (COPD+PAH). Lung tissue from healthy controls, COPD patients, and COPD patients with PAH was used for RT-PCR and histological examination. Results: The serum level of endogenous Apela in COPD+PAH patients was significantly lower than those in the control and COPD groups. Correlation analysis showed that systolic pulmonary artery pressure in COPD+PAH patients was negatively correlated with the serum level of endogenous Apela (r =-0.3842, p < 0.05). The percentage of intima thickening and muscularization of pulmonary arterioles was increased in COPD+PAH patients, while the expression of Apela/APJ was decreased. Compared with the healthy controls and COPD patients, the expression of endothelial markers vWF and CD34 mRNA in the pulmonary arterioles in COPD +PAH patients decreased, while the expression of interstitial markers a-SMA and vimentin mRNA was up -regulated. Conclusion: The present study suggests that expression of the Apela/APJ system is decreased in PAH second-ary to COPD. The pathological changes involved in PAH secondary to COPD include thickening of the intima and muscularization of the pulmonary arterioles, as well as endothelial-to-mesenchymal transition. Corrective action targeting the diminished Apela/APJ system may be a promising therapeutic strategy for PAH in the future. (c) 2023 Elsevier Inc. All rights reserved.