Circulating miR-98-5p serves as a biomarker for older patients with chronic obstructive pulmonary disease and mediates endothelial injury via PRDM1

Chronic obstructive pulmonary disease (COPD) is prevalent in older patients, serving as a primary risk factor for cardiovascular diseases. Considering the widely reported miR-98-5p in respiratory system diseases, it was hypothesized to have great clinical potential in COPD. This study aimed to identify a promising biomarker for older COPD patients, focusing on miR-98-5p. A total of 153 COPD patients (aged over 60 years) were recruited, with 133 healthy individuals as controls. Serum miR-98-5p levels were compared between the two groups, and the clinical potential of miR-98-5p was evaluated in terms of early detection, severity assessment, and MACEs prediction. In vitro, the regulatory effect of miR-98-5p on pulmonary microvascular endothelial injury was investigated with the employment of hPMECs stimulated by CSE. Significant downregulation of miR-98-5p was observed in COPD patients, showing dramatic discriminating potential. Serum miR-98-5p in COPD patients decreased with disease severity and was associated with patients’ pulmonary function. miR-98-5p was also identified as a risk factor for the incidence of MACEs. Downregulation of miR-98-5p was also observed in hPMECs under the treatment of CSE, and its overexpression could alleviate inflammation, improve barrier function, and promote cell viability. PRDM1 was directly targeted by miR-98-5p, which mediates the protective role of miR-98-5p. Reducing miR-98-5p was identified as a potential biomarker assisting in the diagnosis and prognosis prediction of older patients with COPD. Overexpressing miR-98-5p can be a promising therapeutic strategy for preventing barrier dysfunction of hPMECs.