Abstract
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.
Highlights
Hypertension (HTN) is the biggest cause of death all over the world, according to the statistic data, there were a third of adults, approximately 1 billion people in the world that influenced by hypertension, the date of which would enhanced to 1.6 billion by 2025 [1]
The comparison of baseline characteristics between HTN patients and healthy people indicated that there was no obvious difference in age, gender, body mass index (BMI), fasting blood glucose (FBG) and blood urea nitrogen (BUN) between HTN patients and healthy people (P > 0.05); while the difference in high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) was evident between HTN patients and healthy people (Table 1, P < 0.05)
reverse transcription quantitative polymerase chain reaction (RT-qPCR) was employed to evaluate long non-coding RNAs (lncRNAs) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) expression in HTN patients and healthy people to observe the level of lncRNA MALAT1 in HTN patients, the results of which showed that the lncRNA MALAT1 expression of HTN patients was up-regulated compared with healthy controls, suggesting that MALAT1 was highly expressed in the serum of HTN patients (P < 0.05; Figure 1A)
Summary
Hypertension (HTN) is the biggest cause of death all over the world, according to the statistic data, there were a third of adults, approximately 1 billion people in the world that influenced by hypertension, the date of which would enhanced to 1.6 billion by 2025 [1]. The relation www.aging-us.com between lncRNA metastasis-associated lung adenocarcinoma transcript 1(MALAT1) and HTN has not been studied yet. The relation between Notch-1 and HTN has been demonstrated in a recent study that Notch-1 increased proliferation of human pulmonary arterial endothelial cells (hPAECs) in pulmonary arterial hypertension and inhibition of Notch signaling could decrease proliferation and migration of hPAECs [16]. A study has demonstrated that MALAT1 knockdown could enhance chemosensitivity of ovarian cancer cells to cisplatin through inhibiting the Notch-1 signaling pathway [17]. The relation among MALAT1, Notch-1 and HTN has not been studied yet, this study was conducted to focus on the capacity of MALAT1 and Notch-1 in HTN, and we speculated that down-regulated lncRNA MALAT1 could alleviate the vascular lesion and remodeling of HTN rats, the mechanism may be related to the inactivation of Notch signaling pathway
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