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

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.