MiR-483-5p downregulation alleviates ox-LDL induced endothelial cell injury in atherosclerosis.
Atherosclerosis
Autophagy
Endothelial injury
MiR-483-5p
TIMP2
Journal
BMC cardiovascular disorders
ISSN: 1471-2261
Titre abrégé: BMC Cardiovasc Disord
Pays: England
ID NLM: 100968539
Informations de publication
Date de publication:
27 10 2023
27 10 2023
Historique:
received:
12
05
2023
accepted:
04
09
2023
medline:
30
10
2023
pubmed:
28
10
2023
entrez:
27
10
2023
Statut:
epublish
Résumé
In light of the abnormal expression of microRNA (miR-483-5p) in patients with atherosclerosis (AS), its role in vascular endothelial cell injury was explored. And the mechanisms related to autophagy were also elucidated. Human umbilical vein endothelial cells (HUVECs) were given 100 mg/L ox-LDL to induce endothelial injury. Cell transfection was done to regulate miR-483-5p levels. Cell viability and apoptosis were detected. qRT-PCR was employed for the mRNA levels' detection. Autophagic flux impairment of HUVECs was detected after ox-LDL treatment, along with the upregulation of miR-483-5p. Ox-LDL inhibited cell viability and promoted cell apoptosis, but these influences were changed by miR-483-5p downregulation. MiR-483-5p downregulation decreased the mRNA levels of IL-1β, IL-6, ICAM-1 and VCAM-1. 3-MA, the autophagy inhibitor, reversed the beneficial role of miR-483-5p downregulation in ox-LDL-induced HUVECs' injury. TIMP2 acts as a target gene of miR-483-5p, and was downregulated in HUVEC models. MiR-483-5p downregulation alleviated ox-LDL-induced endothelial injury via activating autophagy, this might be related to TIMP2.
Sections du résumé
BACKGROUND
In light of the abnormal expression of microRNA (miR-483-5p) in patients with atherosclerosis (AS), its role in vascular endothelial cell injury was explored. And the mechanisms related to autophagy were also elucidated.
METHODS
Human umbilical vein endothelial cells (HUVECs) were given 100 mg/L ox-LDL to induce endothelial injury. Cell transfection was done to regulate miR-483-5p levels. Cell viability and apoptosis were detected. qRT-PCR was employed for the mRNA levels' detection.
RESULTS
Autophagic flux impairment of HUVECs was detected after ox-LDL treatment, along with the upregulation of miR-483-5p. Ox-LDL inhibited cell viability and promoted cell apoptosis, but these influences were changed by miR-483-5p downregulation. MiR-483-5p downregulation decreased the mRNA levels of IL-1β, IL-6, ICAM-1 and VCAM-1. 3-MA, the autophagy inhibitor, reversed the beneficial role of miR-483-5p downregulation in ox-LDL-induced HUVECs' injury. TIMP2 acts as a target gene of miR-483-5p, and was downregulated in HUVEC models.
CONCLUSION
MiR-483-5p downregulation alleviated ox-LDL-induced endothelial injury via activating autophagy, this might be related to TIMP2.
Identifiants
pubmed: 37891465
doi: 10.1186/s12872-023-03496-1
pii: 10.1186/s12872-023-03496-1
pmc: PMC10612234
doi:
Substances chimiques
oxidized low density lipoprotein
0
MicroRNAs
0
Lipoproteins, LDL
0
RNA, Messenger
0
MIRN483 microRNA, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
521Informations de copyright
© 2023. The Author(s).
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