Long noncoding RNA mediates stroke-induced neurogenesis

Fan, Baoyan; Pan, Wanlong; Wang, Xinli; Wei, Min; He, Annie; Zhao, Anna; Chopp, Michael; Zhang, Zheng Gang; Liu, Xian Shuang

doi:10.1002/stem.3189

Cited by 39 publications

(30 citation statements)

References 61 publications

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“…The lncRNA MALAT-1 has been shown to have neuroprotective effects on spinal cord ischemic/reperfusion injury by regulating miR-204 (Qiao et al, 2018). LncRNAs have also been reported to participate in the regulation of stem cell self-renewal and differentiation in stroke-induced neurogenesis (Fan et al, 2020). Recent studies suggest that lncRNAs are important regulators of the pathophysiological processes of CNS diseases, especially those associated with ischemia; therefore, we are interested in the contribution of lncRNAs to endogenous neurological repair after CCSCI.…”

Section: Introductionmentioning

confidence: 99%

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

Cheng

et al. 2020

Front. Cell Dev. Biol.

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Endogenous repair after chronic compressive spinal cord injury (CCSCI) is of great clinical interest. Ischemia-hypoxia-induced angiogenesis has been proposed to play an important role during this repair process. Emerging evidence indicates that long non-coding RNAs (lncRNAs) are involved in the pathophysiological processes of various diseases. Here, we identified a lncRNA (Xist; X-inactive specific transcript) with upregulated expression in cervical spine lesions during endogenous neurological repair in CCSCI rats. Therapeutically, the introduction of Xist to rats increased neurological function in vivo as assayed using the Basso, Beattie, and Bresnahan (BBB) score and inclined plane test (IPT). We found that the introduction of Xist enhanced endogenous neurological repair by promoting angiogenesis and microvessel density after CCSCI, while depletion of Xist inhibited angiogenesis and cell sprouting and migration. Mechanistically, Xist promoted angiogenesis by sponging miR-32-5p and modulating Notch-1 expression both in vitro and in vivo. These findings suggest a role of the Xist/miR-32-5p/Notch-1 axis in endogenous repair and provide a potential molecular target for the treatment of ischemia-related central nervous system (CNS) diseases.

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Section: Introductionmentioning

confidence: 99%

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

Cheng

et al. 2020

Front. Cell Dev. Biol.

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“…Also, H19 was shown to modulate miRNAs associated with neurogenesis. Notably, functional rehabilitation following stroke was retarded when H19 was blocked in NSCs (Fan et al, 2020). In another investigation, the sensorimotor cortex displayed upregulation of lncRNA H19 expression after MCAO.…”

Section: Lncrnas As Putative Biomarkers and Therapeutic Targetsmentioning

confidence: 95%

“…lncRNA H19 has also been shown to make a significant contribution to stroke pathology. In NSCs isolated from the SVZ of rats afflicted with focal cerebral ischemia, H19 lncRNA expression was significantly increased (Fan et al, 2020). H19 knockdown hindered NSC proliferation and differentiation, along with spurring cell death.…”

Section: Lncrnas As Putative Biomarkers and Therapeutic Targetsmentioning

confidence: 97%

LncRNAs Stand as Potent Biomarkers and Therapeutic Targets for Stroke

Fan

Saft

Sadanandan

et al. 2020

Front. Aging Neurosci.

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Stroke is a major public health problem worldwide with a high burden of neurological disability and mortality. Long noncoding RNAs (lncRNAs) have attracted much attention in the past decades because of their newly discovered roles in pathophysiological processes in many diseases. The abundance of lncRNAs in the nervous system indicates that they may be part of a complex regulatory network governing physiology and pathology of the brain. In particular, lncRNAs have been shown to play pivotal roles in the pathogenesis of stroke. In this article, we provide a review of the multifaceted functions of lncRNAs in the pathogenesis of ischemic stroke and intracerebral hemorrhage, highlighting their promising use as stroke diagnostic biomarkers and therapeutics. To this end, we discuss the potential of stem cells in aiding lncRNA applications in stroke.

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“…Using ChIRP-Western blot and RNA immnunoprecipitation (RIP) assay, chromatin proteins including SUZ12, EZH2 and H3K27me3 were observed to be physically associated with long non-coding RNA (lncRNA) H19, whose association was significantly higher in the ischemic NSCs compared with those from non-ischemic NSCs. Furthermore, our data demonstrate that knockdown of lncRNA markedly reduced levels of EZH2 and H3K27me3 at the promoters of cell cycle-related genes, leading to the upregulation of p27 expression and consequently inhibition of NSC proliferation [ 80 ]. Our novel preliminary data suggest that stroke alters histone factors and thereby the recruitment of epigenetic states to target genes, which underlie stroke-induced neurogenesis.…”

Section: Epigenetics In Adult Neurogenesis After Strokementioning

confidence: 99%

“…In total, 409 mRNAs were identified to be significantly upregulated and 255 were downregulated in ischemic NSCs compared with non-ischemic NSCs. Our study for the first time revealed differential lncRNA profiles and lncRNA–mRNA co-expression network in the NSCs that are associated with stroke-induced neurogenesis [ 80 ]. Furthermore, we demonstrated that the top upregulated lncRNA H19 mediates the proliferation and neuronal differentiation of NSCs by recruiting chromatin remodeling proteins and by regulating miR-675 expression to modulate neurogenesis-related transcription.…”

Section: Epigenetics In Adult Neurogenesis After Strokementioning

confidence: 99%

Epigenetic Mechanisms Underlying Adult Post Stroke Neurogenesis

Liu

Fan

Chopp

et al. 2020

IJMS

Self Cite

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Stroke remains the leading cause of adult disability. Post-stroke neurogenesis contributes to functional recovery. As an intrinsic neurorestorative process, it is important to elucidate the molecular mechanism underlying stroke-induced neurogenesis and to develop therapies designed specifically to augment neurogenesis. Epigenetic mechanisms include DNA methylation, histone modification and its mediation by microRNAs and long-non-coding RNAs. In this review, we highlight how epigenetic factors including DNA methylation, histone modification, microRNAs and long-non-coding RNAs mediate stroke-induced neurogenesis including neural stem cell self-renewal and cell fate determination. We also summarize therapies targeting these mechanisms in the treatment of stroke.

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Long noncoding RNA mediates stroke-induced neurogenesis

Cited by 39 publications

References 61 publications

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

LncRNA Xist Contributes to Endogenous Neurological Repair After Chronic Compressive Spinal Cord Injury by Promoting Angiogenesis Through the miR-32-5p/Notch-1 Axis

LncRNAs Stand as Potent Biomarkers and Therapeutic Targets for Stroke

Epigenetic Mechanisms Underlying Adult Post Stroke Neurogenesis

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