ArticleExperimental and therapeutic medicine2020
Downregulated lncRNA UCA1 accelerates proliferation and migration of vascular smooth muscle cells by epigenetic regulation of MMP9.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- KLF9 aggravates the cardiomyocyte hypertrophy in hypertrophic obstructive cardiomyopathy through the lncRNA UCA1/p27 axis.International journal of experimental pathology · 2025Article
- Genome-wide identification of long noncoding RNA genes and their potential association with mammary gland development in water buffalo.Animal bioscience · 2022Article
- An Unanticipated Modulation of Cyclin-Dependent Kinase Inhibitors: The Role of Long Non-Coding RNAs.Cells · 2022Review
- Epigenetic regulation of gastrointestinal cancers mediated by long non-coding RNAs.Cancer biomarkers : section A of Disease markers · 2022Review
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Authors and funding
7 authors at 3 institutions in 1 country.
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Abstract
Function of long non-coding RNA urothelial carcinoma antigen 1 (lncRNA UCA1) in regulating the proliferative and migratory abilities of vascular smooth muscle cells (VSMCs) by mediating matrix metalloproteinase-9 (MMP9) level were elucidated. After treatment with different concentrations of ox-LDL for different time points, lncRNA UCA1 level in VSMCs was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Subcellular distribution of UCA1 was analyzed. Proliferative and migratory abilities of VSMCs transfected with pcDNA-UCA1 were assessed. Protein level of MMP9 in HA-VSMCs treated with different concentrations of ox-LDL for different time points was also determined. The potential interaction between UCA1 and enhancer of zeste homolog 2 (EZH2) was identified by RNA immunoprecipitation (RIP) assay. Recruitment ability of EZH2 to MMP9 promoter region influenced by UCA1 was determined by Chromatin immunoprecipitation (ChIP) assay. Finally, the potential function of MMP9 in UCA1-mediated cellular behavior of VSMCs was explored. UCA1 was time-dependently and dose-dependently upregulated in VSMCs by ox-LDL treatment. Proliferative and migratory abilities of VSMCs were enhanced by treatment of 100 mg/l ox-LDL for 48 h, which were further reduced after transfection of pcDNA-UCA1. Subcellular distribution analysis showed that UCA1 was mainly distributed in the nucleus. Protein level of MMP9 was gradually elevated with the treatment of increased concentrations of ox-LDL in VSMCs. Its level was downregulated by transfection of pcDNA-UCA1 in VSMCs. The interaction between UCA1 and EZH2 was confirmed by RIP assay. Transfection of pcDNA-UCA1 stimulated the binding of EZH2 on MMP9 promoter region. Finally, overexpression of MMP9 reversed the decreased proliferative and migratory abilities in ox-LDL-treated VSMCs overexpressing UCA1. Downregulated UCA1 accelerates VSMCs to proliferate and migrate through negatively regulating MMP9 level.
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