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. 2021 Mar 26;296:100599. doi: 10.1016/j.jbc.2021.100599

Figure 8.

Figure 8

S1PR2 mediates S1P-induced changes of the STAT3/miR-135b/β-TrCP/YAP/Notch3 signal pathway and PASMCs proliferation. PASMCs were previously treated with JTE013 (10-μM) or CAY10444 (10-μM) for 1 h and then stimulated with S1P, the phosphorylation level of STAT3 (A) and total STAT3 protein level (A), protein levels of β-TrCP (C), YAP (D), Notch3 (E) and NICD3 (E) were examined using Western blotting; β-actin served as a loading control (n = 4 each group); mRNA level of miRNA-135b (B) was detected using qRT-PCR; U6 served as a loading control (n = 3 each group); proliferation of PASMCs (F) was evaluated by the EdU incorporation assay (the scale bar represents 200 μm, n = 3 each group). ∗p < 0.05 versus control, # p < 0.05 versus S1P-treated cells. β-TrCP, β-transduction repeat-containing protein; EdU, 5′-ethynyl-2′-deoxyuridine; NICD3, intracellular domain of the Notch3; PASMCs, pulmonary artery smooth muscle cells; qRT, quantitative real-time; S1P, sphingosine-1-phosphate; STAT3, signal transducers and activators of transcription 3; YAP, yes-associated protein.