Down-regulation of lncRNA MALAT1 alleviates vascular lesion and vascular remodeling of rats with hypertension.
Notch-1
hypertension
lncRNA MALAT1
vascular lesion
vascular remodeling
Journal
Aging
ISSN: 1945-4589
Titre abrégé: Aging (Albany NY)
Pays: United States
ID NLM: 101508617
Informations de publication
Date de publication:
25 07 2019
25 07 2019
Historique:
received:
31
05
2019
accepted:
16
07
2019
pubmed:
26
7
2019
medline:
10
6
2020
entrez:
26
7
2019
Statut:
ppublish
Résumé
Recently, the effect of long non-coding RNAs (lncRNAs) in hypertension (HTN) has been identified. This study aims to explore the expression of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in HTN and its role in vascular lesion and remodeling of HTN rats. LncRNA MALAT1 expression was up-regulated in HTN patients, and lncRNA MALAT1 could be an effective index of HTN diagnosis. Down-regulated MALAT1 and inhibited Notch-1 could reduce relative factor expression, including inflammation-related factors, endothelial function-related factors and oxidative stress-related factors, and inhibit apoptosis of aortic endothelial cells of HTN rats. LncRNA MALAT1 expression in HTN patients and healthy controls was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Angiotensin II (Ang II)-induced HTN rat models were injected with MALAT1-siRNA, empty lentivirus vector, Notch pathway inhibitor (DAPT) and dimethyl sulphoxide (DMSO) via caudal vein. After three-week treatment, changes of blood pressure, inflammatory factor levels, endothelial function-related factors, oxidative stress indices and apoptosis of vascular endothelial cells were determined by a series of assays. This study revealed that down-regulated lncRNA MALAT1 could alleviate the vascular lesion and remodeling of HTN rats, the mechanism may be related to the inhibited activation of Notch signaling pathway.
Identifiants
pubmed: 31343412
doi: 10.18632/aging.102113
pii: 102113
pmc: PMC6682528
doi:
Substances chimiques
MALAT1 long non-coding RNA, human
0
RNA, Long Noncoding
0
RNA, Small Interfering
0
Receptor, Notch1
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
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