Comprehensive analysis of key lncRNAs in ischemic stroke

Chunxiang Fan; Zouqin Huang; Binbin Chen; Baojin Chen; Qi Wang; Weidong Liu; Donghai Yu; Chunxiang Fan; Zouqin Huang; Binbin Chen; Baojin Chen; Qi Wang; Weidong Liu; Donghai Yu

doi:10.3934/mbe.2020066

Mathematical Biosciences and Engineering

2020, Volume 17, Issue 2: 1318-1328. doi: 10.3934/mbe.2020066

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Research article Special Issues

Comprehensive analysis of key lncRNAs in ischemic stroke

1.
TCM Department, Shanghai Punan Hospital of Pudong New Area, Shanghai 200125, China
2.
Department of Acupuncture and Moxibustion, Pudong New Area Hospital of TCM, Shanghai 201299, China
3.
TCM Department, Heqing Community Health Service Center of Pudong New Area, Shanghai 201201, China
4.
Neurosurgery Department, Shanghai Punan Hospital of Pudong New Area, Shanghai 200125, China
5.
TCM Department, Shanghai Seventh People’s Hospital, Shanghai 200137, China

Received: 24 May 2019 Accepted: 31 October 2019 Published: 20 November 2019

Ischemic stroke (IS) is a leading cause of mortality and disability worldwide. However, the treatments for ischemic stroke remained inadequate. The mechanisms underlying ischemic stroke are still not completely understood. the present study identified 19 lncRNAs related to stroke recovery by analyzing a public dataset GSE37587. A co-expression network included 24 lncRNAs, 1668 mRNAs and 3542 edges were constructed in the present study. Bioinformatics analysis showed these lncRNAs were involved in regulating multiple biological processes and pathways, such as mRNA nonsense-mediated decay, translation, cell-cell adhesion. Three lncRNAs, including DLEU1, LOC432369, and LOC338799, were identified as key lncRNAs in stroke. Bioinformatics showed DLEU1 was involved in regulating oxidative phosphorylation, and ubiquitin-mediated proteolysis. LOC432369 was associated with oxidative phosphorylation. LOC338799 was associated with clathrin-dependent endocytosis, the establishment of organelle localization and ribonucleoprotein complex assembly. We thought this study could provide useful information to understand the mechanisms underlying stroke progression.
- long non-coding RNA,
- ischemic stroke,
- co-expression analysis,
- biomarkers
Citation: Chunxiang Fan, Zouqin Huang, Binbin Chen, Baojin Chen, Qi Wang, Weidong Liu, Donghai Yu. Comprehensive analysis of key lncRNAs in ischemic stroke[J]. Mathematical Biosciences and Engineering, 2020, 17(2): 1318-1328. doi: 10.3934/mbe.2020066

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Abstract

Ischemic stroke (IS) is a leading cause of mortality and disability worldwide. However, the treatments for ischemic stroke remained inadequate. The mechanisms underlying ischemic stroke are still not completely understood. the present study identified 19 lncRNAs related to stroke recovery by analyzing a public dataset GSE37587. A co-expression network included 24 lncRNAs, 1668 mRNAs and 3542 edges were constructed in the present study. Bioinformatics analysis showed these lncRNAs were involved in regulating multiple biological processes and pathways, such as mRNA nonsense-mediated decay, translation, cell-cell adhesion. Three lncRNAs, including DLEU1, LOC432369, and LOC338799, were identified as key lncRNAs in stroke. Bioinformatics showed DLEU1 was involved in regulating oxidative phosphorylation, and ubiquitin-mediated proteolysis. LOC432369 was associated with oxidative phosphorylation. LOC338799 was associated with clathrin-dependent endocytosis, the establishment of organelle localization and ribonucleoprotein complex assembly. We thought this study could provide useful information to understand the mechanisms underlying stroke progression.

References

[1]	A. Arboixand and J. Alio, Cardioembolic Stroke: Clinical Features, Specific Cardiac Disorders and Prognosis, Curr. Cardiol. Rev., 6 (2010), 150-161.
[2]	S. Sabour, The Diagnostic Value of Serum miRNA-221-3p, miRNA-382-5p, and miRNA-4271 in Ischemic Stroke: Methodological Issue to Avoid Misinterpretation, J. Stroke Cerebrovasc. Dis., 26 (2017), 1161.
[3]	Z. Wang, Y. Yuan, Z. Zhang, et al., Inhibition of miRNA-27b enhances neurogenesis via AMPK activation in a mouse ischemic stroke model, FEBS Open Bio., 9 (2019), 859-869.
[4]	Z. Wu, P. Wu, X. Zuo, et al., Erratum to: LncRNA-N1LR Enhances Neuroprotection Against Ischemic Stroke Probably by Inhibiting p53 Phosphorylation, Mol. Neurobiol., 54 (2017), 7670-7685.
[5]	J. Wang, B. Cao, D. Han, et al., Long Non-coding RNA H19 Induces Cerebral Ischemia Reperfusion Injury via Activation of Autophagy, Aging Dis., 8 (2017), 71-84.
[6]	J. A. Saugstad, Non-Coding RNAs in Stroke and Neuroprotection, Front. Neurol., 6 (2015), 50.
[7]	T. L. Barr, R. L. Vangilder, S. L. Rellick, et al., A Genomic Profile of the Immune Response to Stroke With Implications for Stroke Recovery, Biol. Res. Nurs., 17 (2015), 248-256.
[8]	X. Wan, W. Huang, S. Yang, et al., Identification of androgen-responsive lncRNAs as diagnostic and prognostic markers for prostate cancer, Oncotarget, 7 (2016), 60503-60518.
[9]	H. Lin, M. Jiang, L. Liu, et al., The long noncoding RNA Lnczc3h7a promotes a TRIM25-mediated RIG-I antiviral innate immune response, Nat. Immunol., 2019 (2019), 1.
[10]	C. H. Liand Y. Chen, Insight Into the Role of Long Noncoding RNA in Cancer Development and Progression, Int. Rev. Cell Mol. Biol., 326 (2016), 33-65.
[11]	H. Yang, X. Xi, B. Zhao, et al., KLF4 protects brain microvascular endothelial cells from ischemic stroke induced apoptosis by transcriptionally activating MALAT1, Biochem. Biophys. Res. Commun., 495 (2018), 2376-2382.
[12]	X. Zhang, X. L. Zhu, B. Y. Ji, et al., LncRNA-1810034E14Rik reduces microglia activation in experimental ischemic stroke, J. Neuroinflammation, 16 (2019), 75.
[13]	D. Wu, Y. C. G. Lee, H. C. Liu, et al., Identification of TLR downstream pathways in stroke patients. Clin. Biochem., 46 (2013):1058-1064.
[14]	X. Wang, S. Cheng, V. H. Brophy, et al., A Meta-Analysis of Candidate Gene Polymorphisms and Ischemic Stroke in 6 Study Populations: Association of Lymphotoxin-Alpha in Nonhypertensive Patients. Stroke, 40 (2009):683-695.
[15]	C. D. Anderson, A. Biffi, M. A. Nalls, et al., Common Variants Within Oxidative Phosphorylation Genes Influence Risk of Ischemic Stroke and Intracerebral Hemorrhage. Stroke, 44 (2013):612-619.
[16]	T. Liu, Z. Han, H. Li, et al., LncRNA DLEU1 contributes to colorectal cancer progression via activation of KPNA3, Mol. Cancer, 17 (2018), 118.
[17]	J. Wang, D. Pappas, P. L. De Jager, et al., Modeling the Cumulative Genetic Risk for Multiple Sclerosis from Genome-Wide Association Data, Genome Med., 3 (2011), 3.
[18]	T. Kim, S. J. Choi, Y. H. Lee, et al., Gene expression profile predicting the response to anti-TNF treatment in patients with rheumatoid arthritis; analysis of GEO datasets, Jt. Bone Spine, 81 (2014), 325-330.
[19]	G. W. E. Santen, M. Kriek and H. Van Attikum, SWI/SNF complex in disorder: SWItching from malignancies to intellectual disability, Epigenetics, 7 (2012), 1219-1224.
[20]	A. Saschen, M. R. Aure, L. Leibovich, et al., LIMT is a novel metastasis inhibiting lncRNA suppressed by EGF and downregulated in aggressive breast cancer, Embo Mol. Med., 8 (2016), 1052-1064.
[21]	J. D. J. Labonne, T. Graves, Y. Shen, et al., A microdeletion at Xq22.2 implicates a glycine receptor GLRA4 involved in intellectual disability, behavioral problems and craniofacial anomalies, BMC Neurol., 16 (2016), 132.

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