ArticleImmunity, inflammation and disease2023
Inhibition of ox-LDL-induced endothelial cell injury by LINC02381 knockdown through the microRNA-491-5p/transcription factor 7 axis.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- MiR-125b-5p ameliorates ox-LDL-induced vascular endothelial cell dysfunction by negatively regulating TNFSF4/TLR4/NF-κB signaling.BMC biotechnology · 2025Article
- Characterizing hub biomarkers for metabolic-induced endothelial dysfunction and unveiling their regulatory roles in EndMT through RNA sequencing and machine learning approaches.Frontiers in cardiovascular medicine · 2025Article
- Inhibition of ox-LDL-induced endothelial cell injury by LINC02381 knockdown through the microRNA-491-5p/transcription factor 7 axis.Immunity, inflammation and disease · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Atherosclerosis (AS) is a complex multifactorial and chronic inflammatory vascular disease that contributes to the development of cardiovascular diseases. Abnormal cellular proliferation in human umbilical vein endothelial cells (HUVECs) is a crucial element in AS development. In this study, we investigated the potential role of the long noncoding RNA LINC02381/microRNA (miR)-491-5p/transcription factor 7 (TCF7) axis in regulating HUVEC injury in 30 participants suffering from AS and 30 healthy control participants. We established an in vitro model of AS in HUVECs using oxidized low-density lipoprotein (ox-LDL), and measured cellular mRNA and protein levels of LINC02381, miR-491-5p, and TCF7 in serum samples using reverse transcription-quantitative polymerase chain reaction and Western blotting assays. We evaluated cell viability, apoptosis, and inflammation using Cell Counting Kit-8, flow cytometry, and enzyme-linked immunosorbent assays, respectively. Moreover, we analyzed apoptosis-related protein expression using western blotting analysis and determined the association between miR-491-5p and LINC02381 or TCF7 using dual-luciferase reporter assay, RNA pull-down, and rescue experiments. We observed that LINC02381 was elevated, while miR-491-5p was downregulated in serum samples from participants with AS and in ox-LDL-treated HUVECs. LINC02381 knockdown was protective against HUVEC injury via miR-491-5p inhibition, which is its downstream target. Rescue experiments further demonstrated that miR-491-5p alleviated HUVEC injury by modulating TCF7. Thus, LINC02381 knockdown ameliorated HUVEC injury by regulating the miR-491-5p/TCF7 axis, which provides new insights into AS treatment strategies.
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