lncRNA ZEB1-AS1 Mediates Oxidative Low-Density Lipoprotein-Mediated Endothelial Cells Injury by Post-transcriptional Stabilization of NOD2

Xu, Xiaohui; Ma, Congmin; Duan, Zhihui; Du, Yanjiao; Liu, Chao

doi:10.3389/fphar.2019.00397

Cited by 16 publications

(9 citation statements)

References 39 publications

(46 reference statements)

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“…[6][7][8] Furthermore, lncRNAs have been reported to play a role in the ox-LDL-induced cell processes associated with human diseases. 9,10 Also, lncRNA OIP5-AS1 promotes the apoptosis of ox-LDL-induced vascular endothelial cells by regulating GSK-3b, 11 meaning that OIP5-AS1 is related to the functional mechanism of ox-LDL. However, the role of OIP5-AS1 in ox-LDL-induced macrophages is unclear.…”

Section: Introductionmentioning

confidence: 99%

Retracted Article: LncRNA OIP5-AS1 contributes to ox-LDL-induced inflammation and oxidative stress through regulating the miR-128-3p/CDKN2A axis in macrophages

Quansheng

Wang

et al. 2019

RSC Adv.

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Section: Introductionmentioning

confidence: 99%

Retracted Article: LncRNA OIP5-AS1 contributes to ox-LDL-induced inflammation and oxidative stress through regulating the miR-128-3p/CDKN2A axis in macrophages

Quansheng

Wang

et al. 2019

RSC Adv.

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“…The report of Xu et al . revealed that Nod2 downregulation could mitigate endothelial cell injury induced by ox-LDL [ 19 ]. Also, the reduction of Nod2 caused by long noncoding RNA XIST inhibition could attenuate endothelial cell injury by repressing apoptosis and promoting the viability of ox-LDL-induced umbilical vein endothelial cells [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

“…It was claimed that Nod2 plays vital roles in the inflammatory process of AS [ 17 ]. Also, Nod2 was revealed to be connected with endothelial cell reactive oxygen species (ROS) generation [ 18 ] and injury [ 19 , 20 ]. However, the molecular mechanisms associated with Nod2 in AS have rarely been reported.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of circular RNA hsa_circ_0003204 inhibits oxidative stress and apoptosis through the miR-330-5p/Nod2 axis to ameliorate endothelial cell injury induced by low-density lipoprotein

Zhang¹,

Zhang²,

Li³

et al. 2021

cejoi

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Introduction: Atherosclerosis (AS) is the leading cause of cardiovascular disease. Circular RNA hsa_circ_0003204 (hsa_circ_0003204) was elevated in oxidized low-density lipoprotein (ox-LDL)induced human umbilical vein endothelial cells. However, the role and molecular mechanism of hsa_circ_0003204 in the AS process have not been studied.Material and methods: Human primary aortic endothelial cells (HAECs) were treated with low-density lipoprotein (ox-LDL) to establish the AS model. The viability of ox-LDL-induced HAECs was assessed by counting kit-8 (CCK8) assay. Reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) levels in ox-LDL-induced HAECs supernatant were evaluated with the relevant kits. The apoptosis of ox-LDL-induced HAECs was determined via flow cytometry assay. The expression of hsa_circ_0003204, miR-330-5p, and nucleotide-binding oligomerization domain 2 (Nod2) was analyzed through quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between hsa_circ_0003204 or Nod2 and miR-330-5p was verified by dual-luciferase reporter assay. Protein level of Nod2 was detected using western blot analysis.Results: Hsa_circ_0003204 and Nod2 were upregulated while miR-330-5p was decreased in ox-LDL-induced HAECs. Hsa_circ_0003204 depletion restrained the oxidative stress and apoptosis of ox-LDL-induced HAECs. Notably, hsa_circ_0003204 regulated Nod2 expression via sponging miR-330-5p in HAECs. Moreover, miR-330-5p inhibition restored the constraint of the oxidative stress and apoptosis of ox-LDL-induced HAECs caused by hsa_circ_0003204 silencing. Additionally, miR-330-5p targeted Nod2 and Nod2 enhancement abolished the repressive effects of miR-330-5p overexpression on the oxidative stress and apoptosis of ox-LDL-induced HAECs.Conclusions: Hsa_circ_0003204 exhaustion mitigated endothelial cell injury through suppressing the oxidative stress and apoptosis in ox-LDL-induced HAECs via the miR-330-5p/Nod2 axis.

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“…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]. The lncRNA NEAT1 has shown that could suppressed the oxidative stress induced injury of vascular endothelial cells by activating the miR181d-5p/CDKN3 [25].…”

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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lncRNA ZEB1-AS1 Mediates Oxidative Low-Density Lipoprotein-Mediated Endothelial Cells Injury by Post-transcriptional Stabilization of NOD2

Cited by 16 publications

References 39 publications

Retracted Article: LncRNA OIP5-AS1 contributes to ox-LDL-induced inflammation and oxidative stress through regulating the miR-128-3p/CDKN2A axis in macrophages

Retracted Article: LncRNA OIP5-AS1 contributes to ox-LDL-induced inflammation and oxidative stress through regulating the miR-128-3p/CDKN2A axis in macrophages

Knockdown of circular RNA hsa_circ_0003204 inhibits oxidative stress and apoptosis through the miR-330-5p/Nod2 axis to ameliorate endothelial cell injury induced by low-density lipoprotein

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

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