ArticleThe Kaohsiung journal of medical sciences2022
The proliferation and migration of atherosclerosis-related HVSMCs were inhibited by downregulation of lncRNA XIST via regulation of the miR-761/BMP9 axis.
Article in The Kaohsiung journal of medical sciences, 2022. 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, 10 citations in OpenAlex.
- The Role of Long Non-Coding RNA in Atherosclerosis: Mechanism and Intervention of Traditional Chinese Medicine.International journal of molecular sciences · 2026Review
- Role of microRNA-761 in modulating laryngeal cancer cell proliferation, metastasis, and apoptosis: regulation of PDCD4 as a key mechanism.Molecular biology reports · 2025Article
- Unveiling the Impact of BMP9 in Liver Diseases: Insights into Pathogenesis and Therapeutic Potential.Biomolecules · 2024Review
- A Review of MicroRNAs and lncRNAs in Atherosclerosis as Well as Some Major Inflammatory Conditions Affecting Atherosclerosis.Biomedicines · 2024Review
- LOXL1-AS1 Aggravates Myocardial Ischemia/Reperfusion Injury Through the miR-761/PTEN Axis.Korean circulation journal · 2023Article
- Long noncoding RNA DANCR expression and its predictive value in patients with atherosclerosis.Bioengineered · 2022Article
- The proliferation and migration of atherosclerosis-related HVSMCs were inhibited by downregulation of lncRNA XIST via regulation of the miR-761/BMP9 axis.The Kaohsiung journal of medical sciences · 2022Article
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Authors and funding
4 authors at 3 institutions in 1 country.
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Abstract
Atherosclerosis (AS) is a chronic inflammatory disease that can be caused by the proliferation and migration of human vascular smooth muscle cells (HVSMCs). Here, we found that lncRNA XIST was related to the abnormal proliferation and migration of HVSMCs, and thus, the mechanism by which XIST regulated HVSMCs was further investigated. HVSMCs were treated with oxidized low-density lipoprotein (ox-LDL, 100 μg/ml) as AS models. CCK8 assays, flow cytometry, Transwell assays and wound healing assays were applied to evaluate cell viability, cell cycle analysis, and cell migration, respectively. A dual-luciferase reporter assay was employed to verify the binding relationships between XIST and miR-761, miR-761, and BMP9. Ox-LDL induced the proliferation and migration of HVSMCs, upregulated the expression of XIST, downregulated miR-761 expression, and activated the BMP9/ALK1/endoglin pathway. Luciferase assays revealed that XIST sponged miR-761. XIST knockdown ameliorated ox-LDL-mediated effects in HVSMCs, which were largely abolished by miR-761 silencing. BMP9 was targeted-inhibited by miR-761. MiR-761 overexpression alleviated ox-LDL-mediated effects in HVSMCs. However, BMP9 overexpression abolished miR-761-mediated effects in HVSMCs treated with ox-LDL. Our findings suggested that XIST knockdown suppressed the proliferation and migration of HVSMCs by promoting miR-761, which targeted-inhibited the BMP9/ALK1/endoglin pathway.
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