LncRNA CRNDE regulates the proliferation and migration of vascular smooth muscle cells

Zhou, Yu; He, Xupeng; Liu, Ruiming; Qin, Yuansen; Wang, Shenming; Yao, Xi; Li, Chunying; Hu, Zhiqiang

doi:10.1002/jcp.28284

Cited by 22 publications

(20 citation statements)

References 32 publications

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“…We obtained ceRNA networks with 8 DElncRNAs, 13 DEmiRNAs, and 19 DEmRNAs. CRANDE plays a role in tumor proliferation, migration, and the occurrence of many other diseases ( Zhou et al, 2019a ; Xie et al, 2020 ). CRANDE interacts with TLR3, and both correlate with advanced disease inflammation in sepsis patients ( Yang et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Integrated Transcriptional Profiling Analysis and Immune-Related Risk Model Construction for Intracranial Aneurysm Rupture

et al. 2021

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Intracranial aneurysms (IAs) may cause lethal subarachnoid hemorrhage upon rupture, but the molecular mechanisms are poorly understood. The aims of this study were to analyze the transcriptional profiles to explore the functions and regulatory networks of differentially expressed genes (DEGs) in IA rupture by bioinformatics methods and to identify the underlying mechanisms. In this study, 1,471 DEGs were obtained, of which 619 were upregulated and 852 were downregulated. Gene enrichment analysis showed that the DEGs were mainly enriched in the inflammatory response, immune response, neutrophil chemotaxis, and macrophage differentiation. Related pathways include the regulation of actin cytoskeleton, leukocyte transendothelial migration, nuclear factor κB signaling pathway, Toll-like receptor signaling pathway, tumor necrosis factor signaling pathway, and chemokine signaling pathway. The enrichment analysis of 20 hub genes, subnetworks, and significant enrichment modules of weighted gene coexpression network analysis showed that the inflammatory response and immune response had a causal relationship with the rupture of unruptured IAs (UIAs). Next, the CIBERSORT method was used to analyze immune cell infiltration into ruptured IAs (RIAs) and UIAs. Macrophage infiltration into RIAs increased significantly compared with that into UIAs. The result of principal component analysis revealed that there was a difference between RIAs and UIAs in immune cell infiltration. A 4-gene immune-related risk model for IA rupture (IRMIR), containing CXCR4, CXCL3, CX3CL1, and CXCL16, was established using the glmnet package in R software. The receiver operating characteristic value revealed that the model represented an excellent clinical situation for potential application. Enzyme-linked immunosorbent assay was performed and showed that the concentrations of CXCR4 and CXCL3 in serum from RIA patients were significantly higher than those in serum from UIA patients. Finally, a competing endogenous RNA network was constructed to provide a potential explanation for the mechanism of immune cell infiltration into IAs. Our findings highlighted the importance of immune cell infiltration into RIAs, providing a direction for further research.

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Section: Discussionmentioning

confidence: 99%

Integrated Transcriptional Profiling Analysis and Immune-Related Risk Model Construction for Intracranial Aneurysm Rupture

et al. 2021

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“…Significantly, the development of restenosis was due to neointima hyperplasia chiefly caused by aberrant VSMC proliferation and migration after vascular wall injury. 28 Although the improvement of drug-eluting stents (DESs) significantly reduced the in-stent stenosis incidence rate by releasing antiproliferative drugs to inhibit VSMC proliferation and migration, it also posed a new problem: late stent thrombosis due to the side effect of antiproliferative drug inevitably suppressing re-endothelialization. 27 Therefore, it is necessary to explore the regulators and molecular mechanisms in VSMC proliferation and migration.…”

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA PEBP1P2 Suppresses Proliferative VSMCs Phenotypic Switching and Proliferation in Atherosclerosis

Lian

Yang

et al. 2020

Molecular Therapy - Nucleic Acids

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Long non-coding RNAs (lncRNAs) play a crucial role in the growth of vascular smooth muscle cells (VSMCs), the dysfunction of which is closely associated with the initiation and progression of cardiovascular diseases (CVDs). Abnormal phenotypic switching and proliferation of VSMCs constitute a significant event in the progression of atherosclerosis. The present study identified a novel lncRNA, PEBP1P2, which serves as a valuable regulator of VSMCs in phenotypic transformation and proliferation. The expression of PEBP1P2 was remarkably decreased in proliferating VSMCs and pathological arteries when using a balloon injury model of rats. Furthermore, we found that PEBP1P2 represses proliferation, migration, and dedifferentiation during phenotype switching in VSMCs induced by platelet-derived growth factor BB (PDGF-BB). Mechanistically, cyclin-dependent kinase 9 (CDK9) was confirmed to be the direct target of PEBP1P2, which was proven to mediate phenotypic switching and proliferation of VSMCs and was rescued by PEBP1P2. Then, we explored the clinical significance, as we observed the decreased expression of PEBP1P2 in the serum of coronary heart disease (CHD) patients and human advanced carotid atherosclerotic plaques. Finally, PEBP1P2 overexpression distinctly suppressed neointima formation and VSMC phenotypic switching in vivo . Taken together, PEBP1P2 inhibits proliferation and migration in VSMCs by directly binding to CDK9, implying that it may be a promising therapeutic target for the treatment of proliferative vascular diseases.

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“…siRNA, microRNA-146a mimics, and microRNA-146a inhibitor were transfected into HK-2 cells using the Lipofectamine 3000 reagent (Thermo Fisher Scientific). The fulllength CRNDE sequence was inserted into the pcDNA3.1 (Invitrogen) vector to construct the pcDNA3.1-CRNDE overexpression plasmid (O/E); the sequence of CRNDE siRNA (si-CRNDE) was sense, GUGCUCGAGUUAAA UTT, anti-sense, AUUACCACGAGCAT [17].…”

Section: Transfection Crnde Expression Plasmid Crndementioning

confidence: 99%

Effects and Mechanism of lncRNA CRNDE on Sepsis-Induced Acute Kidney Injury

Qiu

Wang

et al. 2020

Analytical Cellular Pathology

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Objective. To investigate the effects of lncRNA CRNDE on sepsis-associated acute kidney injury in the human kidney 2 cell line and explore the potential mechanisms. Methods. HK-2 cells were treated with lipopolysaccharides to induce injuries. The expression of CRNDE and miR-146a in HK-2 cells were altered by a transient transfection assay. Cell apoptosis was detected by a flow cytometry assay, and the levels of inflammatory cytokines including TNF-α, IL-6, IL-8, and IL-1β were assessed by ELISA. Furthermore, western blot analysis was performed to detect the expression levels of TLR4/NF-κB pathway-related proteins. And a luciferase reporter gene assay was used to verify if miR-146a was the target of CRNDE. Results. LPS treatment increased CRNDE expression in HK-2 cells. CRNDE overexpression enhanced cell injuries in HK-2 cells significantly increasing inflammatory cytokine levels, including TNF-α, IL-6, IL-8, and IL-1β, and cell apoptosis. In addition, CRNDE overexpression further activated the TLR4/NF-κB pathways in HK-2 cells. Inversely, opposite results were observed in the miR-146a mimic treatment group, and the miR-146a inhibitor could reverse the protein expression changes of TLR4/NF-κB in the si-CRNDE and LPS treatment group. Conclusion. This study demonstrated that CRNDE overexpression could activate the TLR4/NF-κB signaling pathway by regulating miR-146a, which accelerated LPS-induced inflammation and apoptosis in HK-2 cells.

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LncRNA CRNDE regulates the proliferation and migration of vascular smooth muscle cells

Cited by 22 publications

References 32 publications

Integrated Transcriptional Profiling Analysis and Immune-Related Risk Model Construction for Intracranial Aneurysm Rupture

Integrated Transcriptional Profiling Analysis and Immune-Related Risk Model Construction for Intracranial Aneurysm Rupture

Long Non-coding RNA PEBP1P2 Suppresses Proliferative VSMCs Phenotypic Switching and Proliferation in Atherosclerosis

Effects and Mechanism of lncRNA CRNDE on Sepsis-Induced Acute Kidney Injury

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