Identification of potential hub‐lncRNAs in ischemic stroke based on Subpathway‐LNCE method

Zheng, Yanhua; Sun, Shaopeng; Yu, Miao; Fu, Xiuxin

doi:10.1002/jcb.28554

Cited by 14 publications

(14 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…26 A previous report proposed that downregulated NEXN-AS1 might act as a vital biomarker in ischemic stroke. 27 Intriguingly, a recent document manifested that high level of NEXN-AS1 retarded AS progression through repression of adhesion molecules expression and inammatory cytokines secretion by regulating NEXN. 18 These ndings from our study described above prompted us to explore NEXN-AS1 as a potential regulator on VSMC proliferation and migration in AS progression.…”

Section: Discussionmentioning

confidence: 99%

LncRNA NEXN-AS1 attenuates proliferation and migration of vascular smooth muscle cells through sponging miR-33a/b

Zhang

et al. 2019

RSC Adv.

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

LncRNA NEXN-AS1 attenuates proliferation and migration of vascular smooth muscle cells through sponging miR-33a/b

Zhang

et al. 2019

RSC Adv.

View full text Add to dashboard Cite

show abstract

“…It is known that lncRNAs are non-coding segments of RNAs that have notable regulatory functions in the pathophysiological processes of multiple diseases, including OA (13)(14)(15). LINC00473, a novel lncRNA, has been revealed to be upregulated in several diseases, such as ischemic stroke and preeclampsia (16,17). Moreover, LINC00473 is upregulated in patients with severe pain associated with OA (18).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, previous studies have revealed that long intergenic non-protein coding RNA 473 (LINC00473) serves a notable role in various diseases. For example, LINC00473 has been identified as a notable biomarker in ischemic stroke through the subpathway-LNCE method, which was designed to identify lncRNAs that competitively modulated functions in diseases (16). LINC00473 downregulation contributes to the development of preeclampsia (17).…”

Section: Introductionmentioning

confidence: 99%

LINC00473 exacerbates osteoarthritis development by promoting chondrocyte apoptosis and proinflammatory cytokine production through the miR‑424‑5p/LY6E axis

et al. 2021

View full text Add to dashboard Cite

Osteoarthritis (OA) is a common degenerative joint disease that has been identified as one of the major health burdens in aging individuals. Long non-coding RNAs (lncRNAs) participate in the development of diverse diseases, including OA. Among them, lncRNA long intergenic non-protein coding RNA 473 (LINC00473) is one of the few upregulated lncRNAs. The present study aimed to explore the role of LINC00473 and its regulatory mechanism in OA development. Flow cytometry analyses and ELISA were carried out to detect chondrocyte apoptosis and the concentration of proinflammatory cytokines, respectively. The results suggested that LINC00473 knockdown significantly reduced chondrocyte apoptosis and the production of proinflammatory cytokines in IL-1β-stimulated C28/I2 cells compared with transfection with small interfering RNA-negative control (si-NC). Western blot analyses were performed to examine protein levels of apoptotic markers (caspase-3, Bax and Bcl-2) in C28/I2 cells. Subsequently, an OA rat model was established to explore the role of LINC00473 in vivo. The results indicated that, compared with the OA + adeno-associated virus si-NC group, LINC00473 knockdown significantly suppressed the degradation of chondrocyte extracellular matrix and the production of proinflammatory cytokines in OA model rats. Furthermore, bioinformatics analysis, luciferase reporter and RNA immunoprecipitation assays indicated that LINC00473 served as a microRNA (miR)-424-5p sponge in C28/I2 cells, and that lymphocyte antigen 6 locus E (LY6E) was the downstream target. In addition, the inhibitory effects of LINC00473 knockdown on chondrocyte apoptosis and the inflammatory response could be reversed by LY6E overexpression in IL-1β-stimulated C28/I2 cells. In summary, the findings indicated that LINC00473 contributed to OA progression by modulating the miR-424-5p/LY6E axis, which may serve as a potential therapeutic strategy for patients with OA.

show abstract

“…linc-DHFRL1-4, SNHG15, and linc-FAM98A-3 are suggested as biomarkers for the detection of acute IS (Deng et al 2018). Zheng et al (2019) proposed that five lncRNAs, including LINC00265, LINC00473, NEXN-AS1, HCG17, and MEG8, could be considered as important lncRNA biomarkers in IS. In the present study, the area under the ROC curve (AUC) indicated that measuring RUNX1-IT1 in peripheral blood is not suitable for diagnostic purposes in LAA (AUC = 0.609 ± 0.04, sensitivity = 0.59, specificity = 0.61) ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Study and Characterization of Long Non-coding RUNX1-IT1 among Large Artery Atherosclerosis Stroke Patients Based on the ceRNA Hypothesis

et al. 2020

View full text Add to dashboard Cite

Recent studies have shed light on the involvement of long non-coding RNAs (lncRNAs) in the initiation and development of stroke. However, the regulatory function of many lncRNAs in large artery atherosclerosis (LAA) has not been fully elucidated. Based on the competing endogenous RNA (ceRNA) hypothesis recently proposed by Pandolfi, the present study was conducted using experimental techniques and bioinformatics to investigate the expression and regulatory function of a lncRNA involved in the development of LAA. The lncRNAs differentially expressed in stroke were obtained using meta-analysis, and one lncRNA was selected for experimental studies on patients with LAA (n = 100) and healthy controls (n = 100) using quantitative real-time polymerase chain reaction (qRT-PCR). The patients were also evaluated through meta-analysis to identify the function of the selected lncRNA, miRNAs, and mRNAs with altered expression in stroke. Finally, the experimental results and meta-analysis findings were integrated, and different functional groups were assigned. The results indicated that the level of lncRNA-RUNX1-IT1 was significantly lower in the patients with LAA compared to the healthy control subjects (p > 0.05). Logistic regression analyses revealed that the expression of lncRNA-RUNX1-IT1 was inversely correlated with LAA (P = 009, OR = 0.871, 95% CI: 0.786-0.965). In addition, a network of differentially expressed genes (DE genes) was created for miRNAs and mRNAs based on their association with lncRNA-RUNX1-IT1. Functional analysis showed that the DE genes in the network are involved in the apoptosis and alternative splicing of RNAs. The findings of the present study suggest that the downregulation of lncRNA-RUNX1-IT1 is associated with LAA development by interrupting the regulatory network of cells. The results of network analysis demonstrated that the lncRNA-RUNX1-IT1 could influence the expression of mRNAs and miRNAs involved in the apoptosis and alternative splicing of RNAs.

show abstract

Identification of potential hub‐lncRNAs in ischemic stroke based on Subpathway‐LNCE method

Cited by 14 publications

References 25 publications

LncRNA NEXN-AS1 attenuates proliferation and migration of vascular smooth muscle cells through sponging miR-33a/b

LncRNA NEXN-AS1 attenuates proliferation and migration of vascular smooth muscle cells through sponging miR-33a/b

LINC00473 exacerbates osteoarthritis development by promoting chondrocyte apoptosis and proinflammatory cytokine production through the miR‑424‑5p/LY6E axis

Study and Characterization of Long Non-coding RUNX1-IT1 among Large Artery Atherosclerosis Stroke Patients Based on the ceRNA Hypothesis

Contact Info

Product

Resources

About