Key result
Down-regulating lncRNA MALAT1 alleviates vascular lesions and remodeling in hypertensive rats by inhibiting Notch signaling.
Why the study?
The role of lncRNA MALAT1 in hypertension and its effect on vascular lesion and remodeling in hypertensive rats was not fully understood.
Does down-regulation of lncRNA MALAT1 alleviate vascular lesion and remodeling in hypertension models?
Does down-regulation of lncRNA MALAT1 alleviate vascular lesion and remodeling in hypertension models?
Down-regulation of lncRNA MALAT1 alleviates vascular lesions and remodeling in hypertensive rats, likely by inhibiting the Notch signaling pathway.
Should not change hypertension practice; hypothesis-generating for MALAT1-Notch targeting in vascular remodeling.
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.
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Xue et al. (2019) studied Hypertension. MALAT1-siRNA and Notch pathway inhibitor (DAPT) vs. Empty lentivirus vector and DMSO was evaluated on Vascular lesion and remodeling, blood pressure, inflammatory factors, endothelial function, oxidative stress, and apoptosis. Down-regulation of lncRNA MALAT1 alleviated vascular lesions and remodeling in hypertensive rats, likely by inhibiting the Notch signaling pathway.
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