LINC00926 promotes pyroptosis of hypoxia-induced human umbilical vein vascular endothelial cells by recruiting ELAVL1.
10.12122/j.issn.1673-4254.2023.05.17
- Author:
Yong JIANG
1
;
Wenting GE
1
;
Ying ZHAO
2
;
Yuge WU
1
;
Yiming HUO
1
;
Lanting PAN
1
;
Shuang CAO
3
Author Information
1. Department of Laboratory Medicine, Jilin Medical University, Jilin 132013, China.
2. Department of Cardiology, Jilin Central Hospital, Jilin 132011, China.
3. College of Clinical Medicine, Jilin Medical University, Jilin 132013, China.
- Publication Type:Journal Article
- Keywords:
ELAVL1;
coronary heart disease;
human umbilical vein vascular endothelial cells pyroptosis;
lncRNA LINC00926;
- MeSH:
Humans;
Caspase 1;
ELAV-Like Protein 1;
Human Umbilical Vein Endothelial Cells;
Pyroptosis;
RNA, Messenger;
RNA, Long Noncoding/genetics*;
Cell Hypoxia
- From:
Journal of Southern Medical University
2023;43(5):807-814
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the regulatory role of the long non-coding RNA LINC00926 in pyroptosis of hypoxia-induced human umbilical vein vascular endothelial cells (HUVECs) and explore the molecular mechanism.
METHODS:HUVECs were transfected with a LINC00926-overexpressing plasmid (OE-LINC00926), a siRNA targeting ELAVL1, or both, followed by exposure to hypoxia (5% O2) or normoxia. The expression of LINC00926 and ELAVL1 in hypoxia-treated HUVECs was detected using real-time quantitative PCR (RT-qPCR) and Western blotting. Cell proliferation was detected using Cell Counting Kit-8 (CCK-8), and the levels of IL-1β in the cell cultures was determined with ELISA. The protein expression levels of pyroptosis-related proteins (caspase-1, cleaved caspase-1 and NLRP3) in the treated cells were analyzed using Western blotting, and the binding between LINC00926 and ELAVL1 was verified with RNA immunoprecipitation (RIP) assay.
RESULTS:Exposure to hypoxia obviously up-regulated the mRNA expression of LINC00926 and the protein expression of ELAVL1 in HUVECs, but did not affect the mRNA expression of ELAVL1. LINC00926 overexpression in the cells significantly inhibited cell proliferation, increased IL-1β level and enhanced the expressions of pyroptosis-related proteins (all P < 0.05). LINC00926 overexpression further up-regulated the protein expression of ELAVL1 in hypoxia-exposed HUVECs. The results of RIP assay confirmed the binding between LINC00926 and ELAVL1. ELAVL1 knockdown significantly decreased IL-1β level and the expressions of pyroptosis-related proteins in hypoxia-exposed HUVECs (P < 0.05), while LINC00926 overexpression partially reversed the effects of ELAVL1 knockdown.
CONCLUSION:LINC00926 promotes pyroptosis of hypoxia-induced HUVECs by recruiting ELAVL1.
