ArticleChinese medical journal2026
Sphingosine-1-phosphate induces pulmonary artery smooth muscle cell proliferation, migration and pulmonary arterial remodeling by modulating sonic hedgehog signaling effector FoxM1.
Article in Chinese medical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Article
- Sphingosine-1-Phosphate Receptor 1 regulates competition dependent astrocyte morphogenesis and tiling in murine cortex.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSphingosine-1-phosphate (S1P), a metabolite of sphingosine, is associated with the proliferation of pulmonary artery smooth muscle cells (PASMCs). This study aims to address the mechanisms by which S1P induces PASMC proliferation, contributing to pulmonary arterial remodeling.
methodsPrimary cultured rat PASMCs were incubated with S1P. Cyclopamine was used to inhibit Smoothened (SMO) function, while siRNA transfection selectively knocked down the expression of signal transducer and activator of transcription 3 ( STAT3 ), glioma-associated oncogene homolog 1 ( GLI1 ), and forkhead box M1 ( FOXM1 ). Cell proliferation was measured by 5-bromo-2'-deoxyuridine (BrdU) and 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay. Subcellular localization of Gli1 was determined using immunofluorescence staining. In a monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) rat model, PF543 (the inhibitor of S1P synthetase), NSC74859 (the inhibitor of STAT3), and cyclopamine (the inhibitor of sonic hedgehog [Shh] receptor) were administered to evaluate their effects on disease progression. Hemodynamic changes and histological examination were performed to evaluate the development of PAH. The protein levels of sphingosine kinase 1 (SphK1), phosphorylated/total STAT3 (p-/t-STAT3), Shh, Gli1 and FoxM1 were determined using immunoblotting.
resultsS1P increased Shh expression by STAT3 activation, which further caused Gli1 upregulation and nuclear translocation in PASMCs. Activation of Gli1 raised FoxM1 expression and then triggered PASMCs proliferation and migration. In MCT-induced PAH rat models, S1P levels were elevated in lung tissues and serum, triggering STAT3 activation and subsequent upregulation of Shh, Gli1, and FoxM1 in lung. Targeting these molecules alleviated pulmonary arterial remodeling and prevented the development of PAH.
conclusionsS1P/STAT3/Shh/Gli1/FoxM1 pathway plays an important role in PASMCs proliferation and pulmonary arterial remodeling. Targeting this cascade may have potential value for the management of PAH.
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