https://doi.org/10.4081/ejh.2023.3526

LINC00926 is involved in hypoxia-induced vascular endothelial cell dysfunction via miR-3194-5p regulating JAK1/STAT3 signaling pathway

Vol. 67 No. 1 (2023)
Submitted: 12 August 2022
Accepted: 29 December 2022
Published: 16 January 2023
CHD, HUVECs, hypoxia, LINC00926, miR-3194-5p, JAK1, STAT3
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Authors

Yong Jiang
jiangyongpost@sina.com
Department of Laboratory Medicine, Jilin Medical University, Jilin , China.
Chun-hui Xu
Department of Clinical Medicine, Jilin Medical University, Jilin, China.
Ying Zhao
Department of Cardiology, Jilin Central Hospital, Jilin, China.
Yun-han Ji
Department of Laboratory Medicine, Jilin Medical University, Jilin, China.
Xin-tao Wang
Department of Laboratory Medicine, Jilin Medical University, Jilin, China.
Ying Liu
Department of Laboratory Medicine, Jilin Medical University, Jilin, China.

Vascular endothelial cell (VEC) dysfunction is associated with the development of coronary heart disease (CHD). Long intergenic non-protein coding RNA 926 (LINC00926), a kind of long noncoding RNA (lncRNA), has been found to be abnormally expressed in CHD patients. However, the biological role of LINC00926 has not been reported. In our research, we intended to explore the regulatory mechanism of LINC00926 in hypoxia-exposed HUVEC cells (HUVECs). In our in vitro study, HUVECs were exposed under hypoxic conditions (5% O2) for 24 h. RT-qPCR and Western blotting assay were used to detect the mRNA and protein levels. CCK-8 assay, flow cytometry, transwell assay and in vitro angiogenesis assay were performed to measure cell proliferation, apoptosis, migration and tube formation, respectively. Bioinformatics analysis was applied to predict the target of LINC00926 and miR-3194-5p, which was verified by dual-luciferase reporter assays. The results showed that LINC00926 was highly expressed in CHD patients and hypoxia-exposed HUVECs. LINC00926 overexpression suppressed cell proliferation, migration and tube formation and increased cell apoptosis. MiR-3194-5p was a target of LINC00926 and can target binding to JAK1 3’UTR. LINC00926 could up-regulate JAK1 and p-STAT3 levels via miR-3194-5p. In addition, overexpressed LINC00926 suppressed cell proliferation, migration and tube formation and increased cell apoptosis via miR-3194-5p/JAK1/STAT3 axis. In summary, LINC00926 aggravated endothelial cell dysfunction via miR-3194-5p regulating JAK1/STAT3 signaling pathway in hypoxia-exposed HUVECs.

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Ethics Approval

This study was approved by the Ethics Committee of Jilin Medical University

How to Cite

Jiang, Y., Xu, C.- hui ., Zhao, Y. ., Ji, . Y.- han ., Wang, X.- tao ., & Liu, Y. . (2023). LINC00926 is involved in hypoxia-induced vascular endothelial cell dysfunction <em>via</em> miR-3194-5p regulating JAK1/STAT3 signaling pathway. European Journal of Histochemistry, 67(1). https://doi.org/10.4081/ejh.2023.3526
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