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MicroRNA (miR)‑138 serves an important role in the proliferation, differentiation and apoptosis of human pulmonary artery smooth muscle cells (HPASMCs), indi-cating the involvement of miR‑138 in the development and progression of pulmonary artery hypertension (PAH). Potassium channel subfamily K member 3 (TASK‑1), a two‑pore domain K+ channel, is expressed in HPASMCs and is associated with hypoxic PAH. However, whether miR‑138 mediates PAH through targeting TASK‑1 is not known. In the present study, HPASMCs were transfected with miR‑138 mimic to establish a PAH model in vitro, and the effects of a miR‑138 inhibitor and a TASK‑1 inhibitor (A293) were examined. Cell proliferation and mitochondrial membrane potential (MMP) were measured by CCK‑8 assay and flow cytometry, respectively. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to examine the expression of miR‑138, TASK‑1, Bcl‑2, caspase‑3 and activation of extracellular signal‑regulated kinase 1/2 (ERK1/2). A dual‑luciferase reporter assay was also used to analyse the expression level of TASK‑1 in HPASMCs. The results of the present study demonstrated that the miR‑138 mimic promoted proliferation and MMP level, which was similar to the effect of A293 treatment on HPASMCs. However, the miR‑138 inhibitor inhibited the effects induced by miR‑138 mimic or A293 treatment, as demonstrated by a decrease in proliferation and MMP level in HPASMCs, accompanied by a decrease of Bcl‑2 and an increase of caspase‑3 expression levels, as well as ERK1/2 activation. The dual‑luciferase reporter assay indicated that TASK‑1 expression was negatively regulated by miR‑138. The results of the present study suggested that miR‑138 promoted proliferation and suppressed mitochondrial depolarization of HPASMCs by targeting TASK‑1.

MicroRNA‑138 promotes proliferation and suppresses mitochondrial depolarization in human pulmonary artery smooth muscle cells through targeting TASK‑1