Store-operated Ca ²⁺ entry is involved in endothelium-to-mesenchymal transition in lung vascular endothelial cells

EndMT has been reported to contribute to the pathogenesis of PAH. In this study, we aimed to determine the role of Ca ²⁺ signaling in the development of EndMT in human lung vascular endothelial cells. Our data suggest that TGF-β ₁ requires store-operated Ca ²⁺ entry through STIM1/Orai channels to induce SNAI-mediated EndMT. For the first time, we demonstrated that TGF-β ₁ -induced EndMT is a Ca ²⁺ -dependent event, whereas inhibition of STIM1/Orai interaction attenuated EndMT in response to TGF-β ₁ .