Another key observation of the current study indicated that downregulation of MALAT1 or overexpression of miR-150-5p inhibited the apoptosis of HPMECs, suppressed the inflammatory response (reflected by decreased expression of Bax, cleaved caspase 3, IL-6, IL-1β, TNF-α and increased expression of Bcl-2) and decreased the expression of adhesion factors ICAM-1 and E-selectin in vitro, and also alleviated lung injury in ARDS in vivo. Here, BCL2 is linked to acute respiratory distress syndrome.