ArticleThe clinical respiratory journal2024
CircST6GAL1 knockdown alleviates pulmonary arterial hypertension by regulating miR-509-5p/multiple C2 and transmembrane domain containing 2 axis.
Article in The clinical respiratory journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Integrated Analysis of Rat Pulmonary Hypertension Datasets Identifies Candidate circRNA Networks in Hypoxia-Exposed Pulmonary Artery Tissue.International journal of molecular sciences · 2026Article
- The Role of the Apelin Receptor in the Pathophysiology of Pulmonary Arterial Hypertension.Cells · 2026Review
- Targeting CircNLRP12 attenuates hypoxia-induced pulmonary arterial smooth muscle cell dysfunction by sponging miR-107-5p and suppressing the ITGA2-mediated FAK/PI3K/AKT pathway.European journal of medical research · 2025Article
- Focusing on spinal stenosis: emerging discoveries concerning Alendronate-induced risks and genetic drug targets.Journal of orthopaedic surgery and research · 2025Article
- Genome-wide characterization of circular RNAs in three rat models of pulmonary hypertension reveals distinct pathological patterns.BMC genomics · 2025Article
- miRNA regulatory networks as precision diagnostic and therapeutic targets in pulmonary arterial hypertension: from molecular cascades to clinical translation.American journal of cardiovascular disease · 2025Review
- CircST6GAL1 knockdown alleviates pulmonary arterial hypertension by regulating miR-509-5p/multiple C2 and transmembrane domain containing 2 axis.The clinical respiratory journal · 2024Article
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Authors and funding
6 authors.
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Abstract
backgroundHypertension is a main contributing factor of cardiovascular diseases; deregulated circular RNAs are involved in the pathogenesis of pulmonary arterial hypertension (PAH). Herein, we evaluated the function and mechanism of circST6GAL1 in PAH process.
methodsHuman pulmonary artery smooth muscle cells (HPASMCs) were cultured in hypoxic environment for functional analysis. The cell counting kit-8, 5-ethynyl-2'-deoxyuridine, wound healing, and flow cytometry assays were used to investigate cell proliferation, migration, and apoptosis. qRT-PCR and Western blotting analyses were used for level measurement of genes and proteins. The binding between miR-509-5p and circST6GAL1 or multiple C2 and transmembrane domain containing 2 (MCTP2) was analyzed by dual-luciferase reporter, RNA immunoprecipitation, and pull-down assays. The monocrotaline (MCT)-induced PAH mouse models were established for in vivo assay.
resultsCircST6GAL1 was highly expressed in PAH patients and hypoxia-induced HPASMCs. Functionally, circST6GAL1 deficiency reversed hypoxia-induced proliferation and migration, as well as apoptosis arrest in HPASMCs. Mechanistically, circST6GAL1 directly targeted miR-509-5p, and MCTP2 was a target of miR-509-5p. Rescue assays showed that the regulatory effects of circST6GAL1 deficiency on hypoxia-induced HPASMCs were abolished. Moreover, forced expression of miR-509-5p suppressed HPASMC proliferation and migration and induced cell apoptosis under hypoxia stimulation, while these effects were abolished by MCTP2 overexpression. Moreover, circST6GAL1 silencing improved MCT-induced pulmonary vascular remodeling and PAH.
conclusionCircST6GAL1 deficiency reversed hypoxia-induced proliferation and migration, as well as apoptosis arrest in HPASMCs, and alleviated pulmonary vascular remodeling in MCT-induced PAH mouse models through the miR-509-5p/MCTP2 axis, indicating a potential therapeutic target for PAH.
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