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Aging (Albany NY) ; 11(14): 5192-5205, 2019 07 25.
Artículo en Inglés | MEDLINE | ID: mdl-31343412

RESUMEN

OBJECTIVE: 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. RESULTS: 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. METHODS: 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. CONCLUSION: 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.


Asunto(s)
Células Endoteliales/citología , Hipertensión/genética , ARN Largo no Codificante/genética , Remodelación Vascular , Adulto , Anciano , Animales , Apoptosis , Regulación hacia Abajo , Femenino , Humanos , Hipertensión/inducido químicamente , Masculino , Persona de Mediana Edad , ARN Interferente Pequeño , Ratas , Receptor Notch1/metabolismo , Transducción de Señal
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