MicroRNA-301a-3p increases oxidative stress, inflammation and apoptosis in ox-LDL-induced HUVECs by targeting KLF7.
apoptosis
inflammation
microRNA-301a-3p
oxidative stress
oxidized low-density lipoprotein-induced human umbilical vein endothelial cells
Journal
Experimental and therapeutic medicine
ISSN: 1792-0981
Titre abrégé: Exp Ther Med
Pays: Greece
ID NLM: 101531947
Informations de publication
Date de publication:
Jun 2021
Jun 2021
Historique:
received:
22
09
2020
accepted:
08
01
2021
entrez:
14
4
2021
pubmed:
15
4
2021
medline:
15
4
2021
Statut:
ppublish
Résumé
Arteriosclerotic cardiovascular disease is an inflammatory disease of ischemia or endothelial dysfunction caused by atherosclerosis, thereby causing high mortality. The viability and apoptosis of human umbilical vein endothelial cells (HUVECs) following oxidized low-density lipoprotein (ox-LDL) induction or transfection was detected by Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis. MicroRNA (miR)-301a-3p and Krueppel-like factor 7 (KLF7) mRNA expression was determined by reverse transcription-quantitative PCR (RT-qPCR). The levels of monocyte chemoattractant protein-1 (MCP-1) and IL-6, activities of reactive oxygen species and superoxide dismutase and lactate dehydrogenase leakage were analyzed by respective commercial assay kits. The protein expression of IL-6, MCP-1, Bcl2, Bax, poly (ADP-ribose) polymerase (PARP), cleaved PARP, pro-caspase3 and cleaved caspase-3 was detected by western blotting. miR-301a-3p expression is highly expressed in ox-LDL-induced HUVECs. miR-301a-3p is also a target of KLF7. Inhibition of miR-301a-3p suppressed oxidative stress, inflammation and apoptosis in ox-LDL-induced HUVECs, which was reversed by KLF7 inhibition. In conclusion, miR-301a-3p promotes oxidative stress, inflammation and apoptosis in ox-LDL-induced HUVECs via decreasing KLF7 expression.
Identifiants
pubmed: 33850541
doi: 10.3892/etm.2021.10001
pii: ETM-0-0-10001
pmc: PMC8027757
doi:
Types de publication
Journal Article
Langues
eng
Pagination
569Informations de copyright
Copyright: © Jiang et al.
Déclaration de conflit d'intérêts
The authors declare they have no competing interests.
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