circRNA/lncRNA-miRNA-mRNA Network in Oxidized, Low-Density, Lipoprotein-Induced Foam Cells

Wang, Libo; Zheng, Zhaoshi; Feng, Xia‐Ting; Zang, Xuege; Ding, Wenyuan; Wu, Fan; Zhao, Qini

doi:10.1089/dna.2019.4865

Cited by 54 publications

(35 citation statements)

References 47 publications

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“…With the rapid development of high-throughput sequencing and other biotechnologies, numerous circRNAs have been found in various organisms, such as nematodes, fruit flies, mice, macaques, and humans. Further studies have revealed that circRNAs play important roles in the occurrence and development of cancer, nervous system diseases, cardiovascular diseases, and metabolic diseases (Wang et al, 2019 ; Xiao, 2020 ).…”

Section: The Role Of Noncoding Rna In β Cell Differentiation and Funcmentioning

confidence: 99%

RETRACTED: Roles of Epigenetic Modifications in the Differentiation and Function of Pancreatic β-Cells

Liu

et al. 2020

Front. Cell Dev. Biol.

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Diabetes, a metabolic disease with multiple causes characterized by high blood sugar, has become a public health problem. Hyperglycaemia is caused by deficiencies in insulin secretion, impairment of insulin function, or both. The insulin secreted by pancreatic β cells is the only hormone in the body that lowers blood glucose levels and plays vital roles in maintaining glucose homeostasis. Therefore, investigation of the molecular mechanisms of pancreatic β cell differentiation and function is necessary to elucidate the processes involved in the onset of diabetes. Although numerous studies have shown that transcriptional regulation is essential for the differentiation and function of pancreatic β cells, increasing evidence indicates that epigenetic mechanisms participate in controlling the fate and regulation of these cells. Epigenetics involves heritable alterations in gene expression caused by DNA methylation, histone modification and non-coding RNA activity that does not result in DNA nucleotide sequence alterations. Recent research has revealed that a variety of epigenetic modifications play an important role in the development of diabetes. Here, we review the mechanisms by which epigenetic regulation affects β cell differentiation and function.

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Section: The Role Of Noncoding Rna In β Cell Differentiation and Funcmentioning

confidence: 99%

RETRACTED: Roles of Epigenetic Modifications in the Differentiation and Function of Pancreatic β-Cells

Liu

et al. 2020

Front. Cell Dev. Biol.

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“…Furthermore, circRNAs can serve as a competitive endogenous RNA (ceRNA) to sponge miRNAs to regulate the target mRNAs (14,15). To describe the role of circRNA-0006896 during the progression of carotid plaque destabilization, bioinformatics analysis was used to predict the potential target miRNAs of circRNA-0006896 and construct a circRNA-miRNA network map associated with AS.…”

Section: Rt-qpcr Validation Prediction Of Mrna-mirna-circrna Relatiomentioning

confidence: 99%

“…circRNAs can sponge miRNAs through stable complementary binding and regulate gene expression. Numerous studies have demonstrated that circRNAs are stable and abundant within exosomes; moreover, they may be key to the mechanisms through which exosomes promote certain disease (1,14,15).…”

Section: Introductionmentioning

confidence: 99%

circRNA‑0006896‑miR1264‑DNMT1 axis plays an important role in carotid plaque destabilization by regulating the behavior of endothelial cells in atherosclerosis

et al. 2021

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Atherosclerosis (AS) is a chronic inflammatory disease of the vascular wall with multiple causes. AS is the primary pathological basis of cardiovascular disease and stroke. Moreover, carotid plaque rupture and thrombus formation are the main causes of ischemic stroke. Therefore, understanding the formation of carotid plaques may help improve the prediction and prevention of cardiovascular and cerebrovascular events. Endothelial cell dysfunction results in re-endothelialization and angiogenesis in atherosclerotic plaques, thus promoting plaque destabilization. The aim of the present study was to evaluate the effect of circular RNA (circRNA) molecules in serum exosomes (serum-Exos) from patients with stable plaque atherosclerosis (SA) and unstable/vulnerable plaque atherosclerosis (UA). Specifically, the effect of circRNA on human umbilical vein endothelial cell (HUVEC) behavior and the mechanisms underlying plaque destabilization in AS were evaluated. Serum-Exos were isolated, then identified using transmission electron microscopy, nanoparticle tracking analysis and western blotting. The serum-Exo-circRNA expression profile of patients with SA or UA was investigated using a circRNA array. The relationship between circRNA-006896 in serum-Exos and biochemical parameters of patients with SA and UA were analyzed using Spearman's correlation. In addition, HUVECs were incubated with serum-Exos for in vitro functional assays. The present study demonstrated that circRNAs expression profiles in SA and UA serum-Exos were significantly different, indicating a potential role for circRNAs in carotid plaque destabilization. The expression of circRNA-0006896 was positively correlated with triglyceride, low-density lipoprotein cholesterol (LDL-C) and C-reactive protein levels, and negatively correlated with albumin levels in patients with UA. However, circRNA-0006896 expression was positively correlated with LDL-C in patients with SA. Using bioinformatic analysis, a competing endogenous RNA (ceRNA) network was selected to study the regulatory roles of circRNA-0006896 in serum-Exos. Additionally, in HUVECs treated with serum-Exos derived from patients with UA, the expression of circRNA-0006896 in HUVECs was upregulated. This was accompanied by decreased expression of microRNA-1264 and SOCS3, increased levels of DNMT1 and phosphorylated STAT3. HUVEC proliferation and migration were significantly increased in the UA group, compared with the mock and SA groups. This finding indicates that the circRNA-0006896-miR-1264-DNMT1 axis plays an important role in carotid plaque destabilization by regulating the behavior of endothelial cells. Moreover, it suggests that circRNA-0006896 may represent a therapeutic target for controlling JNK/STAT3 signaling in HUVECs. Thus, this study may provide insight on potential interventions against vulnerable plaque formation in patients with AS.

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“…A loop of has-circ-0028198/has-circ-0092317/XIST/miR- Fig. 6 In RA-FLSs, upregulated PVT1 enhanced SCUBE2 expression by sponging miR-543, thereby facilitating cell proliferation and suppressing apoptosis via the enhancement of PCNA, Ki67, and Bcl2 expression, as well as promoting the production of IL-1β 543/aspartate beta-hydroxylase or has-circ-0028198/hascirc-0092317/XIST/miR-543/phosphodiesterase 3B has been implicated in oxidized, low-density, lipoproteinstimulated foam cells in atherosclerosis [24]. Furthermore, miR-543 was significantly reduced under senescence-inducing conditions and could modulate the aging process of human mesenchymal stem cells [25].…”

Section: Discussionmentioning

confidence: 99%

Knockdown of long non-coding RNA PVT1 induces apoptosis of fibroblast-like synoviocytes through modulating miR-543-dependent SCUBE2 in rheumatoid arthritis

Wang

Kong

et al. 2020

J Orthop Surg Res

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Background: Rheumatoid arthritis (RA), a kind of autoimmune disorder, is featured by many physical symptoms and proliferation of fibroblast-like synoviocytes (FLSs). The relevance of long non-coding RNAs (lncRNAs) in the progression of RA has been probed. Hence, the goal of this report was to investigate the action of plasmacytoma variant translocation 1 (PVT1), a lncRNA, in FLSs and the basic mechanism. Methods: Initially, RA rats were developed to evaluate the expression of PVT1, microRNA-543 (miR-543), and signal peptide-CUB-EGF-like containing protein 2 (SCUBE2) in synovial tissues. Enhancement or loss of PVT1 or miR-543 was achieved to explore their effects on proliferation, cell cycle, and apoptosis of FLSs. The interaction between PVT1 and miR-543 and between miR-543 and its putative target SCUBE2 was examined to elucidate the correlations. Finally, the protein expression of proliferation-and apoptosis-associated genes were assessed by western blot assays. Results: PVT1 was overexpressed in synovial tissues from RA patients through microarray expression profiles. The PVT1 and SCUBE2 expression was boosted, and miR-543 was reduced in synovial tissues of rats with RA. PVT1 specifically bound to miR-543, and miR-543 negatively regulated SCUBE2 expression. Overexpression of PVT1 or silencing of miR-543 enhanced SCUBE2 expression, thereby promoting proliferation and interleukin-1β (IL-1β) secretion, while inhibiting apoptosis rate of FLSs. Conversely, si-SCUBE2 reversed the role of miR-543 inhibitor. Conclusion:The key findings support that PVT1 knockdown has the potency to hinder RA progression by inhibiting SCUBE2 expression to sponge miR-543.

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circRNA/lncRNA-miRNA-mRNA Network in Oxidized, Low-Density, Lipoprotein-Induced Foam Cells

Cited by 54 publications

References 47 publications

RETRACTED: Roles of Epigenetic Modifications in the Differentiation and Function of Pancreatic β-Cells

RETRACTED: Roles of Epigenetic Modifications in the Differentiation and Function of Pancreatic β-Cells

circRNA‑0006896‑miR1264‑DNMT1 axis plays an important role in carotid plaque destabilization by regulating the behavior of endothelial cells in atherosclerosis

Knockdown of long non-coding RNA PVT1 induces apoptosis of fibroblast-like synoviocytes through modulating miR-543-dependent SCUBE2 in rheumatoid arthritis

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