LncRNA MACC1-AS1 attenuates microvascular endothelial cell injury and promotes angiogenesis under hypoxic conditions via modulating miR-6867-5p/TWIST1 in human brain microvascular endothelial cells

Yan, Gong; Zhao, Hongyang; Xiao, Hong

doi:10.21037/atm-20-4915

Cited by 28 publications

(16 citation statements)

References 39 publications

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“…The researchers found that lncRNA HULC was associated with high risk, severe illness, and poor prognosis in patients with acute ischemic stroke ( 40 ). LncRNA MACC1-AS1 alleviated microvascular endothelial cell injury, promoted angiogenesis by regulating mir-6867-5p/TWIST1, and played a protective role in ischemic stroke ( 41 ). In addition, the researchers found that lncRNA RMRP had a protective effect on ischemic stroke by activating the PI3K/Akt signaling pathway through valproate ( 42 ).…”

Section: Discussionmentioning

confidence: 99%

Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p

et al. 2021

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Ischemic stroke is one of the main causes of physical disability and mortality worldwide. Long non-coding RNAs (lncRNAs) are reported to be dysregulated in various biological progressions and serve important roles in pathological processes of cerebral ischemia. However, their biological actions and potential mechanisms in the progression of ischemic stroke remain unknown. The present study aimed to investigate the functions of LINC00319 on ischemic brain injury. It was identified that LINC00319 was significantly upregulated in the Gene Expression Omnibus profile of ischemic stroke. Furthermore, LINC00319 overexpression elevated caspase-3 activity and increased the apoptotic rate of neuronal cells, as well as decreased cell viability and glucose uptake. It was also demonstrated that LINC00319 participated in oxygen-glucose deprivation (OGD)-induced cerebral ischemic injury. LINC00319 could competitively bind with microRNA (miR)-200a-3p and decrease its expression. Moreover, miR-200a-3p could partly offset the negative effects of LINC00319 overexpression on neuronal injury caused by OGD. Collectively, the present results suggested that LINC00319 promoted apoptosis and aggravated neuronal injury induced by OGD by regulating miR-200a-3p, which may be important for ischemic stroke treatment.

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Section: Discussionmentioning

confidence: 99%

Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p

et al. 2021

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“…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). For example, Yan et al (2020) showed that LncRNA MACC1-AS1 acts as a ceRNA for miR-6867-5p to regulate TWIST1 to promote cell proliferation, migration and angiogenesis. found that overexpression of lncRNA DANCR enhanced survival and angiogenesis in OGD-treated BMECs through the miR-33a-5p/XBP1s axis.…”

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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“…Then, streptavidin agarose beads (Invitrogen, Carlsbad, CA, USA) were incubated with the cell lysates, and the RNA complex that bound to the beads was eluted and puri ed using TRIzol reagent (Takara, Shiga, Japan). Gene level in the RNA complex was analyzed by RT-qPCR 26 .…”

Section: Rna Pull-downmentioning

confidence: 99%

Silencing lncRNA HOTAIR improves the recovery of neurological function in ischemic stroke via the miR-148a-3p/KLF6 axis

Huang

Wang

Liu

et al. 2021

Brain Research Bulletin

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Ischemic stroke (IS), caused by a permanent or transient local reduction in blood supply to the brain, is one of the most widespread causes of public health problems in modern society. Long non-coding RNA (LncRNA) has been reported to be related to angiogenesis following IS. In this study, we explored the effect and potential molecular mechanism of lncRNA HOTAIR in IS. Permanent middle cerebral artery occlusion (pMCAO) model and oxygen and glucose deprivation (OGD) model were established. HOTAIR was increased in vivo and in vitro models post-ischemic. HOTAIR knockdown promoted neurological function recovery, manifesting in decreased modi ed neurological severity score, cerebral infarcted area, apoptosis and in ammation, and improved balance ability, spatial learning and memory ability. Silencing HOTAIR also improved the viability of OGD-induced N2a cells, and attenuated apoptosis and in ammation. HOTAIR can compete with KLF6 to bind to miR-148a-3p. miR-148a-3p knockdown or KLF6 overexpression partially reversed the effect of sh-HOTAIR on OGD-induced N2a cells. HOTAIR suppressed the activation of STAT3 pathway via the miR-148a-3p/KLF6 axis. To summarize, this study demonstrated that lncRNA HOTAIR absorbed miR-148a-3p and up-regulate KLF6 expression through ceRNA mechanism, and inhibited STAT3 pathway, promoted apoptosis and in ammation, and aggravated neurological injury post-IS.

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LncRNA MACC1-AS1 attenuates microvascular endothelial cell injury and promotes angiogenesis under hypoxic conditions via modulating miR-6867-5p/TWIST1 in human brain microvascular endothelial cells

Cited by 28 publications

References 39 publications

Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p

Upregulated LINC00319 aggravates neuronal injury induced by oxygen‑glucose deprivation via modulating miR‑200a‑3p

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

Silencing lncRNA HOTAIR improves the recovery of neurological function in ischemic stroke via the miR-148a-3p/KLF6 axis

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