Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53

Song, Jingwen; Huang, Songqun; Wang, Kaizhong; Li, Wei; Pao, Lizhi; Chen, Feng; Zhao, Xianxian

doi:10.3389/fgene.2019.00078

Cited by 18 publications

(10 citation statements)

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“…Ang II plays a role in endothelial dysfunction and it induced endothelial dysfunction is closely associated with cardiovascular diseases [ 16 ]. Previous studies have shown that Ang II-induced endothelial dysfunction has been used in hypertension models [ 17 , 18 ]. Autophagy plays a protective effect against endothelial injury by degrading damaged proteins and organelles and recycling the components for use in subsequent cellular processes [ 19 , 20 ].…”

Section: Discussionmentioning

confidence: 99%

Ibandronate promotes autophagy by inhibiting Rac1–mTOR signaling pathway in vitro and in vivo

et al. 2022

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We previously reported that ibandronate (IBAN) could improve endothelial function in spontaneously hypertensive rats. However, the mechanism by which IBAN improves endothelial function is unclear. The IBAN-induced autophagic process in vitro experiments were determined by detection of LC3, Beclin1, and P62 protein levels via western blotting. The autophagy flux was detected by confocal microscopy and transmission electron microscopy. For in vivo experiments, spontaneously hypertensive rats were orally administered with IBAN. Utilizing angiotensin II (Ang II) to stimulate the human umbilical vein endothelial cells (HUVECs) and human pulmonary microvascular endothelial cells (HPMECs) as a model of endothelial cell injury in hypertension, we found that IBAN promoted autophagy and protected cell viability in Ang II-treated-endothelial cells while these effects could be reversed by autophagy inhibitor. In terms of mechanism, IBAN treatment decreased the levels of Rac1 and mammalian target of rapamycin (mTOR) pathway. Activating either Rac1 or mTOR could reverse IBAN-induced autophagy. Furthermore, the in vivo experiments also indicated that IBAN promotes autophagy by downregulating Rac1-mTOR. Taken together, our results firstly revealed that IBAN enhances autophagy via inhibiting Rac1-mTOR signaling pathway, and thus alleviates Ang II-induced injury in endothelial cells.

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Section: Discussionmentioning

confidence: 99%

Ibandronate promotes autophagy by inhibiting Rac1–mTOR signaling pathway in vitro and in vivo

et al. 2022

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“…Therefore, stimulation of HUVECs with Ang II is a reliable model to simulate vascular endothelial injury in vitro . In previous studies, the concentration and dose time of Ang II in an in vitro model were different ( 29 , 30 ). As presented in Fig.…”

Section: Discussionmentioning

confidence: 99%

Peptidomics analysis revealed that a novel peptide VMP‑19 protects against Ang II‑induced injury in human umbilical vein endothelial cells

Ding

Zhang

et al. 2021

Mol Med Rep

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Vascular endothelial dysfunction is a vital pathological change in hypertension, which is mainly caused by apoptosis and oxidative stress injury of vascular endothelial cells. Peptidomics is a method for the direct analysis of small bioactive peptides in various biological samples using liquid chromatography-mass spectrometry (MS)/MS. Given the advantages of the low molecular weight, optimum targeting and easy access to cells, peptides have attracted extensive attention in the field of drug research. However, to the best of our knowledge, little is currently known regarding the role of peptides in vascular endothelial injury. In order to investigate the peptides involved in vascular endothelial protection, MS was used to analyze the peptide profiles in the supernatant of human umbilical vein endothelial cells (HUVECs) stimulated by Ang II. The results revealed that 211 peptides were identified, of which six were upregulated and 13 were downregulated when compared with the control group. Subsequently, the present study analyzed the physical and chemical properties and biological functions of identified peptides by bioinformatics, and successfully screened a peptide (LLQDSVDFSLADAINTEFK) named VMP-19 that could alleviate the apoptosis and oxidative stress injury of HUVECs induced by Ang II. In conclusion, to the best of our knowledge, the present study was the first to use peptidomics to analyze the peptide profiles of supernatant secreted by HUVECs, and revealed that the novel peptide VMP-19 could protect HUVECs from apoptosis and oxidative stress injury. The results of the present study could provide novel insights into treatment strategies for hypertension.

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“…There are already some studies revealed that the relationship between the lncRNA and the vascular endothelial cells injury. For instance, the lncRNA Meg3 was consider as a protective element during the injury process of the vascular endothelial cells [23]. However, the lncRNA ZEB1-AS1 enhanced the oxidative low-density lipoprotein induced damage of the vascular endothelial cells [24].…”

Section: Discussionmentioning

confidence: 99%

Knockdown of Long Noncoding RNA (lncRNA) AK094457 Relieved Angiotensin II Induced Vascular Endothelial Cell Injury

Sun

2020

Med Sci Monit

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Departmental sources Background: Hypertension could induce many serious diseases, including damage to vascular endothelial cells. As a noncoding RNA, long noncoding RNA (lncRNA) has received much attention in scientific research and has a regulating efficacy on many critical life activities in human body. The level of lncRNA AK094457 is thought to be elevated in hypertensive rats. However, there is no research indicating the relationship between the level of lncRNA AK094457 and vascular endothelial injury. Material/Methods: In our study, we used lentiviral to knockdown lncRNA AK094457, and the human umbilical vein endothelial cells (HUVECs) were stimulated by the Ang II to imitate the vascular endothelial cell damage caused by hypertension. The Cell Counting Kit-8 assays were used to detect the cells viability. Western blotting was performed to detect the endothelial nitric oxide synthase (eNOS), p-eNOS and endothelin-1 (ET-1). After that the production of the NO was monitored. At last, the reactive oxygen species (ROS) levels and apoptosis rates were detected in this study. Results: According to the results, we found that knockdown lncRNA AK094457 could alleviate the decrease of vascular endothelial cell viability induced by angiotensin II (Ang II). The knockdown of lncRNA AK094457 also relieved the downregulation of eNOS and p-eNOS, and the decreasing of NO release. At the same time, the knockdown of lncRNA inhibited the levels of Ang II-induced proinflammatory cytokines (tumor necrosis factor [TNF]-a, interleukin [IL]-1, and IL-6) and cell adhesion molecules (vascular cell adhesion molecule 1 [VCAM-1], intercellular adhesion molecule 1 [ICAM-1], and monocyte chemoattractant protein-1 [MCP-1]). The levels of ROS and apoptosis rates also decreased after the knockdown of lncRNA AK094457. Conclusions: All these results indicated that lncRNA AK094457 could promote Ang II-induced vascular endothelial cell injury. On the contrary, knockdown of lncRNA AK094457 could alleviate this damage.

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Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53

Cited by 18 publications

References 50 publications

Ibandronate promotes autophagy by inhibiting Rac1–mTOR signaling pathway in vitro and in vivo

Ibandronate promotes autophagy by inhibiting Rac1–mTOR signaling pathway in vitro and in vivo

Peptidomics analysis revealed that a novel peptide VMP‑19 protects against Ang II‑induced injury in human umbilical vein endothelial cells

Knockdown of Long Noncoding RNA (lncRNA) AK094457 Relieved Angiotensin II Induced Vascular Endothelial Cell Injury

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