Long noncoding RNA CASC2 inhibits ox-LDL-mediated vascular smooth muscle cells proliferation and migration via the regulation of miR-532-3p/PAPD5

Wang, Chenjing; Nan, Xiaodong; Guo, Zhong; Huang, Shuangsheng; Wang, Xiaokun; Feng, Sun; Ma, Shanshan

doi:10.1186/s10020-020-00200-3

Cited by 15 publications

(8 citation statements)

References 29 publications

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“…miRNA-532 is associated with vulnerable plaques and modified low-density lipoprotein or tumor necrosis factor α exposure. The lncRNA CASC2 suppresses cell proliferation and promotes apoptosis by regulating the miR-532–3p/PAPD5 axis in ox-LDL-mediated VSMCs ( Wang et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Contribution of FBLN5 to Unstable Plaques in Carotid Atherosclerosis via mir128 and mir532–3p Based on Bioinformatics Prediction and Validation

Yue

et al. 2022

Front. Genet.

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FBLN5, a member of the short fibulins in the fibulin family of extracellular matrix/matricellular proteins, is involved in interactions with components of the basement membrane and extracellular matrix proteins. It plays key roles in endothelial tissues in many vascular diseases. In this study, the relationship between FBLN5 and carotid atherosclerotic plaque stability as well as the regulatory roles of miRNAs were evaluated. Differential gene expression analyses and weighted gene co-expression network analysis (WGCNA) based on the GSE163154 dataset (including 16 samples without intraplaque hemorrhage and 27 samples with intraplaque hemorrhage) in GEO revealed that FBLN5 is related to plaque stability and is the most significantly differentially expressed gene. LASSO regression was used to evaluate genes obtained from the intersection of differentially expressed genes and clinically significant modules identified by WGCNA. A prediction model based on eight genes, including FBLN5, was constructed and showed an accuracy of 0.951 based on an ROC analysis. Low FBLN5 expression in plaque tissues was confirmed by immunohistochemistry and western blotting. GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analyses showed that FBLN5 acted mainly by the maintenance of the cellular matrix and reactive oxygen species production. miRNAs upstream of these eight predictive genes, including FBLN5, were identified and used to construct a network diagram. These results revealed that hsa-mir-128 and hsa-mir-532–3p were upstream regulatory factors of FBLN5, as verified by PCR assays of human plaque tissues demonstrating that both miRNAs were significantly up-regulated. Therefore, FBLN5 may play an important role in carotid atherosclerosis via hsa-mir-128 and hsa-mir-532–3p as well as become an essential target for treatment.

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Section: Discussionmentioning

confidence: 99%

Contribution of FBLN5 to Unstable Plaques in Carotid Atherosclerosis via mir128 and mir532–3p Based on Bioinformatics Prediction and Validation

Yue

et al. 2022

Front. Genet.

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“…It could be due to (a) difference in the platforms for analyzing the miRNAs expression, (b) difference in the methodology used for normalization, and (c) biological difference due to the use of independent samples in qRT-PCR and NGS. Recently, in isoproterenol-treated H9C2 cells, miR-532-3p was reported to be downregulated and its overexpression was found to reduce the cell apoptosis [53]. On the contrary, in animal model of type 2 diabetes and left ventricle samples of diabetic patients, miR-532-3p was reported to be upregulated and its suppression was found to reduce high-glucose-induced apoptosis [54].…”

Section: Discussionmentioning

confidence: 99%

Investigating microRNAs in diabetic cardiomyopathy as tools for early detection and therapeutics

Mathur

Saxena

2022

Mol Cell Biochem

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To profile microRNAs population of glucose-induced cardiomyoblast cell line and identify the differentially expressed microRNAs and their role under pre-diabetes and diabetes condition in vitro. Rat fetal ventricular cardiomyoblast cell line H9c2 was treated with d-glucose to mimic pre-diabetic, diabetic, and high-glucose conditions. Alteration in cellular, nuclear morphology, and change in ROS generation was analyzed through fluorescent staining. Small RNA sequencing was performed using Illumina NextSeq 550 sequencer and was validated using stem-loop qRT-PCR. A large number (~ 100) differential miRNAs were detected in each treated samples as compared to control; however, a similar expression pattern was observed between pre-diabetes and diabetes conditions with the exception for miR-429, miR-101b-5p, miR-503-3p, miR-384-5p, miR-412-5p, miR-672-5p, and miR-532-3p. Functional annotation of differential expressed target genes revealed their involvement in significantly enriched key pathways associated with diabetic cardiomyopathy. For the first time, we report the differential expression of miRNAs (miR-1249, miR-3596d, miR-3586-3p, miR-7b-3p, miR-191, miR-330-3p, miR-328a, let7i-5p, miR-146-3p, miR-26a-3p) in diabetes-induced cardiac cells. Hyperglycemia threatens the cell homeostasis by dysregulation of miRNAs that begins at a glucose level 10 mM and remains undetected. Analysis of differential expressed miRNAs in prediabetes and diabetes conditions and their role in regulatory mechanisms of diabetic cardiomyopathy holds high potential in the direction of using miRNAs as minimally invasive diagnostic and therapeutic tools.

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“…On the contrary, Wang et al reported that miR-532-3p had a promotion effect on hepatocellular carcinoma proliferation and metastasis [ 30 ]. MiR-532-3p had been shown to promote ox-LDL-induced vascular smooth muscle cells proliferation and migration [ 31 ]. The dysregulation of miR-532-3p-CSF2RA axis was associated with vulnerable plaque formation [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Circ_0000064 promotes high glucose-induced renal tubular epithelial cells injury to facilitate diabetic nephropathy progression through miR-532-3p/ROCK1 axis

Wang

Huang

et al. 2022

BMC Endocr Disord

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Background Circular RNA (circRNA) has been shown to mediate diabetic nephropathy (DN) development by regulating renal tubular epithelial cells (RTECs) injury. However, the role and mechanism of circ_0000064 in high glucose (HG)-induced RTECs injury have not been fully elucidated. Methods Human RTECs (HK-2) were exposed to HG to induce cell injury. Cell oxidative stress was assessed by detecting the levels of oxidative stress-markers. Moreover, cell proliferation and apoptosis were determined by CCK8 assay, EDU assay and flow cytometry. The protein levels of proliferation markers, apoptosis markers and Rho-associated coiled-coil-containing kinase 1 (ROCK1) were measured using western blot analysis. Furthermore, quantitative real-time PCR was performed to assess the expression of circ_0000064, microRNA (miR)-532-3p and ROCK1. The interaction between miR-532-3p and circ_0000064 or ROCK1 was confirmed by dual-luciferase reporter assay and RNA pull-down assay. Results Our results revealed that HG treatment could promote HK-2 cells oxidative stress, apoptosis, fibrosis, and inhibit proliferation. Circ_0000064 expression was increased in the serum of DN patients and HG-induced HK-2 cells, and silenced circ_0000064 could relieve HG-induced HK-2 cells injury. MiR-532-3p could be sponged by circ_0000064, and its overexpression also alleviated HG-induced HK-2 cells injury. Besides, the regulation of circ_0000064 knockdown on HG-induced HK-2 cells injury could be reversed by miR-532-3p inhibitor. Additionally, ROCK1 was a target of miR-532-3p, and its expression was inhibited by circ_0000064 knockdown. The inhibition effect of circ_0000064 knockdown on HG-induced HK-2 cells injury also could be reversed by overexpressing ROCK1. Conclusion In summary, circ_0000064 knockdown might alleviate HG-induced HK-2 cells injury via regulating the miR-532-3p/ROCK1 axis, which provided a new perspective for DN treatment.

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Long noncoding RNA CASC2 inhibits ox-LDL-mediated vascular smooth muscle cells proliferation and migration via the regulation of miR-532-3p/PAPD5

Cited by 15 publications

References 29 publications

Contribution of FBLN5 to Unstable Plaques in Carotid Atherosclerosis via mir128 and mir532–3p Based on Bioinformatics Prediction and Validation

Contribution of FBLN5 to Unstable Plaques in Carotid Atherosclerosis via mir128 and mir532–3p Based on Bioinformatics Prediction and Validation

Investigating microRNAs in diabetic cardiomyopathy as tools for early detection and therapeutics

Circ_0000064 promotes high glucose-induced renal tubular epithelial cells injury to facilitate diabetic nephropathy progression through miR-532-3p/ROCK1 axis

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