Circ_0065149 Alleviates Oxidized Low-Density Lipoprotein-Induced Apoptosis and Inflammation in Atherosclerosis by Targeting miR-330-5p

Li, Dan; Wen, Ji; Sun, Liguang; Wu, Jiawei; Hu, Hao; Ma, Likun

doi:10.3389/fgene.2021.590633

Cited by 13 publications

(15 citation statements)

References 23 publications

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“…A recent study has shown that oxLDL treatment leads to decreased expression of circ_0065149. However, overexpression of circ_0065149 leads to inhibition of NF-κB p65 subunit and the expression of IL-6 and IL-1β ( 51 ). These evidences suggest that genetic or epigenetic regulation of endothelial inflammation represents a promising way to attenuate endothelial dysfunction and atherosclerosis with several large-scale clinical trials discussed the efficacy of anti-inflammatory therapies in cardiovascular medicine, targeting IL-1β and IL-6.…”

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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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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“…miR-330-5p is also reported to modulate inflammation and cell apoptosis. In atherosclerosis, circ_0065149 alleviates oxidized low-density lipoprotein-induced apoptosis and inflammation by targeting miR-330-5p [ 42 ]. In addition, most existing studies have shown that miR-330-5p plays an important role in the regulation of metastatic invasion and epithelial-mesenchymal transformation in tumors [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA BIRF Promotes Brain Ischemic Tolerance Induced By Cerebral Ischemic Preconditioning Through Upregulating GLT-1 via Sponging miR-330-5p

Zhang

Lin

et al. 2022

Mol Neurobiol

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Long noncoding RNAs (lncRNAs) play an important regulatory role in various diseases. However, the role of lncRNAs in brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIPC) is still unknown. The lncRNA profile of rat cortical astrocytes pretreated with ischemic preconditioning was analyzed by high-throughput sequencing. The results of Cell-Counting Kit-8 (CCK-8) assay showed that a novel lncRNA, NONRATT009133.2, which we referred to as brain ischemia–related factor (BIRF), was highly correlated with BIT. Through bioinformatics analysis, we predicted that BIRF, miR-330-5p, and GLT-1 (also named Slc1a2) might constitute a ceRNA regulatory network in the induction of BIT. We found that BIRF was upregulated by CIPC, which promoted GLT-1 expression and BIT induction. BIRF could directly bind to miR-330-5p. Furthermore, miR-330-5p directly targeted GLT-1, and miR-330-5p inhibited both GLT-1 expression and BIT induction in vitro and in vivo. Moreover, BIRF acts as a molecular sponge to competitively bind to miR-330-5p with GLT-1 mRNA, while the miR-330-5p inhibitor reversed all the effects of BIRF siRNA on GLT-1 expression and neuronal vitality. Taken together, our results demonstrate the important roles of the BIRF/miR-330-5p/GLT-1 axis in the induction of BIT by CIPC. BIRF may be a potentially effective therapeutic strategy against stroke injury.

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“…apoptosis of oxLDL-stimulated endothelial cells [210][211][212], macrophages [213,214], and VSMCs [215,216].…”

Section: Discussionmentioning

confidence: 99%

“…CircRNAs are stable and rich in miR-binding sites that serve as miR sponges or competitive endogenous RNAs. Currently, it has been shown that they are able to modulate the proliferation, migration, inflammatory response, and apoptosis of oxLDL-stimulated endothelial cells [ 210 , 211 , 212 ], macrophages [ 213 , 214 ], and VSMCs [ 215 , 216 ].…”

Section: The Oxldl Signalingmentioning

confidence: 99%

Oxidized LDLs as Signaling Molecules

2021

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Levels of oxidized low-density lipoproteins (oxLDLs) are usually low in vivo but can increase whenever the balance between formation and scavenging of free radicals is impaired. Under normal conditions, uptake and degradation represent the physiological cellular response to oxLDL exposure. The uptake of oxLDLs is mediated by cell surface scavenger receptors that may also act as signaling molecules. Under conditions of atherosclerosis, monocytes/macrophages and vascular smooth muscle cells highly exposed to oxLDLs tend to convert to foam cells due to the intracellular accumulation of lipids. Moreover, the atherogenic process is accelerated by the increased expression of the scavenger receptors CD36, SR-BI, LOX-1, and SRA in response to high levels of oxLDL and oxidized lipids. In some respects, the effects of oxLDLs, involving cell proliferation, inflammation, apoptosis, adhesion, migration, senescence, and gene expression, can be seen as an adaptive response to the rise of free radicals in the vascular system. Unlike highly reactive radicals, circulating oxLDLs may signal to cells at more distant sites and possibly trigger a systemic antioxidant defense, thus elevating the role of oxLDLs to that of signaling molecules with physiological relevance.

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Circ_0065149 Alleviates Oxidized Low-Density Lipoprotein-Induced Apoptosis and Inflammation in Atherosclerosis by Targeting miR-330-5p

Cited by 13 publications

References 23 publications

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

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

LncRNA BIRF Promotes Brain Ischemic Tolerance Induced By Cerebral Ischemic Preconditioning Through Upregulating GLT-1 via Sponging miR-330-5p

Oxidized LDLs as Signaling Molecules

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