Exosomes-Mediated LncRNA ZEB1-AS1 Facilitates Cell Injuries by miR-590-5p/ETS1 Axis Through the TGF-β/Smad Pathway in Oxidized Low-density Lipoprotein-induced Human Umbilical Vein Endothelial Cells

Chen, Difang; Wang, Kunwei; Zheng, Yan; Wang, Guangyu; Jiang, Mei

doi:10.1097/fjc.0000000000000974

Cited by 17 publications

(10 citation statements)

References 30 publications

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“…Contradictorily, a study of miRNA expression profile has shown that miR-590-5p is overexpressed in squamous cell carcinoma and functions as the tumor promoter [ 23 ]. In addition, miR-590-5p is downregulated in oxidized low density lipoprotein- (ox-LDL-) induced HUVECs, and the overexpression of miR-590-5p inhibits the apoptosis of HUVECs induced by ox-LDL [ 24 ]. In this study, we found that miR-590-5p overexpression promoted cell proliferation and induced cell apoptosis in A β -induced BV-2 and HT22 cells, which suggested that miR-590-5p exhibited protective effect against cell injury induced by A β .…”

Section: Discussionmentioning

confidence: 99%

miR-590-5p Overexpression Alleviates β-Amyloid-Induced Neuron Damage via Targeting Pellino-1

Lin

Peng

Chen

et al. 2022

Analytical Cellular Pathology

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Alzheimer’s disease (AD) is one common degenerative disorder. However, the effects of miR-590-5p on AD and the mechanism on modulation of AD development were unclear. In this study, the miR-590-5p level in AD patients at mild, moderate, and severe stage as well as APP/PS1 transgenic mice was detected by qRT-PCR. The relationship of miR-590-5p and pellino-1 (PELI1) was identified by double luciferase reporter gene assay. Afterwards, both BV-2 and HT22 cells were exposed to β-amyloid (Aβ) peptides to mimic AD cell model. Then, the roles of miR-590-5p upregulation or PELI1 silence in cell proliferation and apoptosis were explored by CCK-8 assay and TUNEL assay, and the expression of apoptosis-related proteins was detected by western blotting. Furthermore, the involvements of the downstream Traf3/MAPK P38 pathway with the roles of miR-590-5p in AD were measured by western blotting. Our results showed that knockdown of miR-590-5p was found in AD patients, mice model, and Aβ-induced cell model. Notably, PELI1 was proved as a target gene of miR-590-5p. miR-590-5p mimic or PELI1 silence significantly promoted cell proliferation and inhibited cell apoptosis, as well as suppressed the activation of Traf3/MAPK P38 pathway both in Aβ-induced BV-2 and HT22 cells. The effects of PELI1 overexpression on cell proliferation, apoptosis, and Traf3/MAPK P38 pathway were partly abrogated by miR-590-5p mimic both in BV-2 and HT22 cells. In conclusion, miR-590-5p was expressed at lower levels in AD, and miR-590-5p/PELI1 axis might be involved in the progression of AD by the downstream Traf3/MAPK P38 pathway.

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Section: Discussionmentioning

confidence: 99%

miR-590-5p Overexpression Alleviates β-Amyloid-Induced Neuron Damage via Targeting Pellino-1

Lin

Peng

Chen

et al. 2022

Analytical Cellular Pathology

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“…Similarly, the ZEB1-AS1 was also observed to participate in the endothelial injury induced by oxLDL with its increasing expression dose-independently and the further increasing levels of ROS and MDA, through the upregulating HMGB1 with the sponge of miR-942 and contributes to the apoptosis of endothelial cells ( 30 ). The exosome-mediated ZEB1-AS1 was also shown to facilitate cellular injury via signaling mediated with miR-590-5p and ETS1, and the pathway with TGF-β and Smad participated in oxLDL induced HUVECs ( 31 ). The inhibition of NEAT1 and the myocardial infarction-associated transcript (MIAT) expression in the oxLDL-induced model had also been reported to repress the endothelial dysfunction while their molecular pathways are quietly different.…”

Section: Oxldl and Endothelial Cell Dysfunctionmentioning

confidence: 99%

Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis

Jiang

Zhou

Nabavi³

et al. 2022

Front. Cardiovasc. Med.

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Atherosclerosis is an immuno-metabolic disease involving chronic inflammation, oxidative stress, epigenetics, and metabolic dysfunction. There is compelling evidence suggesting numerous modifications including the change of the size, density, and biochemical properties in the low-density lipoprotein (LDL) within the vascular wall. These modifications of LDL, in addition to LDL transcytosis and retention, contribute to the initiation, development and clinical consequences of atherosclerosis. Among different atherogenic modifications of LDL, oxidation represents a primary modification. A series of pathophysiological changes caused by oxidized LDL (oxLDL) enhance the formation of foam cells and atherosclerotic plaques. OxLDL also promotes the development of fatty streaks and atherogenesis through induction of endothelial dysfunction, formation of foam cells, monocyte chemotaxis, proliferation and migration of SMCs, and platelet activation, which culminate in plaque instability and ultimately rupture. This article provides a concise review of the formation of oxLDL, enzymes mediating LDL oxidation, and the receptors and pro-atherogenic signaling pathways of oxLDL in vascular cells. The review also explores how oxLDL functions in different stages of endothelial dysfunction and atherosclerosis. Future targeted pathways and therapies aiming at reducing LDL oxidation and/or lowering oxLDL levels and oxLDL-mediated pro-inflammatory responses are also discussed.

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“…Ni et al discussed the relationship between exocrine-derived non-coding RNAs (lncRNAs and miRNAs) in endothelial cells and vascular smooth muscle cells and their mechanism in vascular senescence (39). Recently, Cheng et al found in vitro that the exo-lncRNA ZEB1-AS1 secreted by human umbilical vein endothelial cells induced by oxidized low-density lipoprotein (ox-LDL) enhances the damage caused by the MIR-590-5P/ETS1 axis to human umbilical vein endothelial cells through the TGF-β/Smad pathway (40). Current studies have shown that exosomal lncRNAs participate in the dynamic evolution of underlying cardiovascular diseases through various pathways, involving all aspects of their pathophysiology and potential treatment.…”

Section: Exosomal Lncrna In Cardiovascular Diseasementioning

confidence: 99%

New Developments in Exosomal lncRNAs in Cardiovascular Diseases

Yuan

Huang

2021

Front. Cardiovasc. Med.

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Long non-coding RNAs (lncRNAs) are non-coding RNAs with lengths >200 nt and are involved in the occurrence and development of cardiovascular diseases (CVDs). Exosomes are secreted and produced by various cell types. Exosome contents include various ncRNAs, proteins and lipids. Exosomes are also important mediators of intercellular communication. The proportion of lncRNAs in exosomes is low, but increasing evidence suggests that exosomal lncRNAs play important roles in CVDs. We focused on research progress in exosomal lncRNAs in atherosclerosis, myocardial infarction, myocardial ischemia-reperfusion injury, cardiac angiogenesis, cardiac aging, rheumatic heart disease, and chronic kidney disease combined with CVD. The potential diagnostic and therapeutic effects of exosomal lncRNAs in CVDs are summarized based on preclinical studies involving animal and cell models and circulating exosomes in clinical patients. Finally, the challenges and possible prospects of exosomes and exosomal lncRNAs in clinical applications related to CVD are discussed.

show abstract

Exosomes-Mediated LncRNA ZEB1-AS1 Facilitates Cell Injuries by miR-590-5p/ETS1 Axis Through the TGF-β/Smad Pathway in Oxidized Low-density Lipoprotein-induced Human Umbilical Vein Endothelial Cells

Cited by 17 publications

References 30 publications

miR-590-5p Overexpression Alleviates β-Amyloid-Induced Neuron Damage via Targeting Pellino-1

miR-590-5p Overexpression Alleviates β-Amyloid-Induced Neuron Damage via Targeting Pellino-1

Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis

New Developments in Exosomal lncRNAs in Cardiovascular Diseases

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