Galectin‐3 mediates pulmonary vascular endothelial cell dynamics via TRPC1/4 under acute hypoxia

Abstract Galectin‐3 (Gal‐3) has been implicated in various biological functions, yet little is known about its role in regulating the dynamics of pulmonary vascular endothelial cells. Gal‐3 was shown to be increased in hypoxic model rats by sequencing analysis. We exposed pulmonary vessel endothelial cells (PVECs) to hypoxia or Gal‐3 stimulation, following which cell apoptosis and autophagy were measured with the relevant methods. The results demonstrated that hypoxia elevated nuclear factor‐κB (NF‐κB) activity and Gal‐3 expression. Gla‐3 decreased the expression of Bcl‐2, Alix, Beclin‐1, Atg5, and LC3A/B. The messenger RNA and protein levels of transient receptor potential channel 1/4 (TRPC1/4) and calpain were reduced after Gal‐3 treatment. Gal‐3 also activated protein kinase B/glycogen synthase kinase‐3 β/mammalian target of rapamycin signaling pathways in PVECs. These results suggest that a hypoxia‐mediated increase in Gal‐3 promotes apoptosis and inhibits autophagy by inhibiting the TRPC1/4 pathway and activating the protein kinase B/glycogen synthase kinase‐3 β/mammalian target of rapamycin signaling pathway in PVECs. Furthermore, these results may provide us with a new direction to explore the pathogenesis of pulmonary artery hypertension.