MALAT1 Protected the Angiogenesis Function of Human Brain Microvascular Endothelial Cells (HBMECs) Under Oxygen Glucose Deprivation/re-oxygenation (OGD/R) Challenge by Interacting with miR-205-5p/VEGFA Pathway

Gao, Chang; Zhang, Cui-Cui; Yang, Hao-Xiang; Hao, Yongnan

doi:10.1016/j.neuroscience.2020.03.027

Cited by 24 publications

(13 citation statements)

References 28 publications

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“…Moreover, mechanistic studies have suggested that Snhg1 targets miR-338a and regulates HIF-1α and VEGF expression ( Wang Z. et al, 2018 ). It has been reported that LncRNA MALAT1 protected against angiogenesis in HBMECs under OGD conditions via the miR-205-5p/VEGFA axis ( Gao C. et al, 2020 ). Additionally, LncRNA metastasis-associated colon cancer 1 (MACC1)-AS1, which sponges miR-6867-5p/TWIST1, regulates the proliferation, survival, and migration of hypoxic HBMECs( Yan G. et al, 2020 ).…”

Section: Regulatory Roles Of Lncrnas In Bmecsmentioning

confidence: 99%

“…MALAT1 expression is upregulated after OGD/R treatment in neurons, BV-2 cells, and astrocytes, which results in MALAT1 acting as a harmful factor in I/R injury by promoting cell death via apoptosis and inflammation ( Guo et al, 2017 ; Wang H. et al, 2020 ; Zhang G. et al, 2020 ; Cao et al, 2020 ; Jia et al, 2021 ). However, MALAT1 plays a protective role in BMECs subjected to OGD/R because it reduces apoptosis and promotes angiogenesis ( Li Z. et al, 2017 ; Gao C. et al, 2020 ; Gao and Wang 2020 ). In summary, the roles of LncRNA MALAT1 in IS include a protective effect on endothelial cells; however, it may induce cell death in neurons and astrocytes.…”

Section: Lncrnas In the Neurovascular Unitmentioning

confidence: 99%

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Long Non-Coding RNA-Mediated Competing Endogenous RNA Networks in Ischemic Stroke: Molecular Mechanisms, Therapeutic Implications, and Challenges

Zhang

Zhu

et al. 2021

Front. Pharmacol.

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Ischemic stroke (IS) is a disease that is characterized by high mortality and disability. Recent studies have shown that LncRNA-mediated competing endogenous RNA (ceRNA) networks play roles in the occurrence and development of cerebral I/R injury by regulating different signaling pathways. However, no systematic analysis of ceRNA mechanisms in IS has been reported. In this review, we discuss molecular mechanisms of LncRNA-mediated ceRNA networks under I/R injury. The expression levels of LncRNAs, microRNAs (miRNAs), and messenger RNAs (mRNAs) and their effects in four major cell types of the neurovascular unit (NVU) are also involved. We further summarize studies of LncRNAs as biomarkers and therapeutic targets. Finally, we analyze the advantages and limitations of using LncRNAs as therapeutics for IS.

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Section: Regulatory Roles Of Lncrnas In Bmecsmentioning

confidence: 99%

Section: Lncrnas In the Neurovascular Unitmentioning

confidence: 99%

Long Non-Coding RNA-Mediated Competing Endogenous RNA Networks in Ischemic Stroke: Molecular Mechanisms, Therapeutic Implications, and Challenges

Zhang

Zhu

et al. 2021

Front. Pharmacol.

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“…Similarly, the overexpression of MALAT1 was associated with increased angiogenesis and cell proliferation. Furthermore, it was also shown that MALAT1 acted as a ceRNA of miR-205-5p, which is able to upregulate VEGFA [62]. Consequently, these studies have confirmed that lncRNA MALAT1 is able to protect the angiogenesis function in ischemic conditions via the regulation of different miRNAs, which are henceforth able to upregulate pro-angiogenic factors ( Fig.…”

Section: Lncrna Malat1mentioning

confidence: 59%

Long Non-coding RNAs as Promising Therapeutic Approach in Ischemic Stroke: a Comprehensive Review

et al. 2020

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In recent years, ischemic stroke (IS) has been one of the major causes of disability and mortality worldwide. The general mechanism of IS is based on reduced blood supply to neuronal tissue, resulting in neuronal cell damage by various pathological reactions. One of the main techniques for acute IS treatment entails advanced surgical approaches for restoration of cerebral blood supply but this is often associated with secondary brain injury, also known as ischemic reperfusion injury (I/R injury). Many researches have come to emphasize the significant role of long non-coding RNAs (lncRNAs) in IS, especially in I/R injury and their potential as therapeutic approaches. LncRNAs are non-protein transcripts that are able to regulate cellular processes and gene expression. Further, lncRNAs have been shown to be involved in neuronal signaling pathways. Several lncRNAs are recognized as key factors in the physiological and pathological processes of IS. In this review, we discuss the role of lncRNAs in neuronal injury mechanisms and their association with brain neuroprotection. Moreover, we identify the lncRNAs that show the greatest potential as novel therapeutic approaches in IS, which therefore merit further investigation in preclinical research.

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“…Angiogenesis is an important part of cerebral ischemia repair, and promoting angiogenesis is considered a promising strategy for the treatment of ischemic stroke (Sun et al 2020;Wlodarczyk et al 2021). Numerous studies have shown that non-coding RNAs, such as miRNAs and lncRNAs, play a critical role in IS angiogenesis (Gao et al 2020;Heydari et al 2020). Nowadays, increasing evidence also suggests a complex and close relationship between miRNAs and lncRNAs, based on Salmena's hypothesis that lncRNAs may attract miRNAs as molecular sponges and participate in IS angiogenesis by regulating the expression of downstream genes through miRNAs (Mengqi Zhang and Xinyi Lv 2020; Yan et al 2020).…”

Section: Discussionmentioning

confidence: 99%

Construction of a Competitive Endogenous RNA Network Associated with Angiogenesis in Ischemic Stroke Using a Bioinformatics Approach

Wang

Zhang

Xie

et al. 2021

Preprint

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Ischemic stroke (IS) is one of the leading causes of death and disability worldwide, and angiogenesis is an important target for its treatment. However, the mechanism of angiogenesis of endogenous RNA (ceRNA) in IS remains poorly understood. This study aims to explore the role of ceRNA in the angiogenesis of IS, to provide a possible target for the treatment of IS. First, GSE22255 (mRNA), GSE55937 (miRNA) and GSE102541 (lncRNA) were downloaded from the Gene Expression Omnibus (GEO) database. Then, a total of 21 mRNA modules were identified by WGCNA analysis, among which NR4A1, PTGS2, ERG3, and VEGFA in cyan module were identified as key genes for angiogenesis. Subsequently, 1454 differentially expressed lncRNAs (DELs) were screened and a lncRNA-mRNA co-expression network consisting of 40 lncRNAs and 4 mRNAs was constructed by correlation analysis. Then, 16 differentially expressed miRNAs (DEMs) were screened and the online database was used to predict the interaction information between miRNAs, lncRNAs and mRNAs. The angiogenesis-related ceRNA network was finally constructed based on ceRNA theory, in which 1 DEL was predicted as a ceRNA for 2 DEMs to regulate 4 hub genes, specifically, HCG18-has-let-7i-5p-NR4A1/PTGS2/ERG3, HCG18-miR-148a-3p-PTGS2/ERG3/VEGFA interaction axis. The results of gene set enrichment analysis (GSEA) suggest that HCG18 may regulate angiogenesis through NF-kB-TNFA signaling pathway, hypoxia and other pathways. In conclusion, the above genes may be new biomarkers and potential targets for the treatment of IS.

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MALAT1 Protected the Angiogenesis Function of Human Brain Microvascular Endothelial Cells (HBMECs) Under Oxygen Glucose Deprivation/re-oxygenation (OGD/R) Challenge by Interacting with miR-205-5p/VEGFA Pathway

Cited by 24 publications

References 28 publications

Long Non-Coding RNA-Mediated Competing Endogenous RNA Networks in Ischemic Stroke: Molecular Mechanisms, Therapeutic Implications, and Challenges

Long Non-Coding RNA-Mediated Competing Endogenous RNA Networks in Ischemic Stroke: Molecular Mechanisms, Therapeutic Implications, and Challenges

Long Non-coding RNAs as Promising Therapeutic Approach in Ischemic Stroke: a Comprehensive Review

Construction of a Competitive Endogenous RNA Network Associated with Angiogenesis in Ischemic Stroke Using a Bioinformatics Approach

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