Knockdown of lncRNA SNHG15 Ameliorates Oxygen and Glucose Deprivation (OGD)-Induced Neuronal Injury via Regulating the miR-9-5p/TIPARP Axis

Shen, Bin; Wang, Lan; Xu, Yuejun; Wang, Hongwei; He, Shiyi

doi:10.1007/s10528-021-10121-3

Cited by 6 publications

(5 citation statements)

References 29 publications

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“…This indicated that SNHG15 probably improve apoptosis through regulating autophagy. A previous study by Shen showed that knock-out of SNHG15 could induce injury of N-2a cells and inhibited apoptosis through inhibiting OGD, this was consistent with the present study [22]. The present study further detect autophagy and found that knock-out of SNHG15 may improve apoptosis through inhibiting autophagy.…”

Section: Discussionsupporting

confidence: 91%

LncRNA SNHG15 regulates autophagy and prevents from cerebral ischemia-reperfusion injury through mediating miR-153-3p/ATG5 axis

Yu¹,

Cai²,

Zhou³

2023

Preprint

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Background: Ischemic stroke is a common cerebrovascular disease. Long noncoding RNA (lncRNA) of small nucleolar RNA host gene (SNHG15) has been supposedly performed a regulatory role in many diseases. Nonetheless, the function of SNHG15 in cerebral ischemia-reperfusion injury has not been clarified. Method: The OGD/R of Neuro2A cells simulated the ischemic and reperfused states of the brain. Neuro2a cell line with stable transfection of plasmid with silent expression of SNHG15 was constructed. Neuro2a cell lines transfected with miR-153-3p mimic (miR-153-3p-mimics) and miR-153-3p inhibitor (miR-153-3p-inhibition) were constructed. Expression of SNHG15, mi R-200a, FOXO3 and ATG7 in mouse brain tissue and N2a cells were able to be identified by qRT-PCR. Western blot (WB) analysis of mouse brain tissue and Neuro2a cells revealed the presence of the proteins ATG5, Cle-caspase-3, Bax, Bcl-2, LC3 II/I, and P62 (WB). The representation and distribution of LC3B were observed by immunofluorescence. The death of cells was measured using a technique called flow cytometry (FACS). Results: SNHG15 was highly expressed in cerebral ischemia-reperfusion injury model. Down regulation of SNHG15 lead to lower apoptosis rate and decreased autophagy. Dual luciferase assay and co-immunoprecipitation (CoIP) found lncRNA SNHG15/miR-153-3p/ATG5. Compared to cells transfected with NC suppression, cells transfected with miR-153-3p-inhibition had substantially greater overexpression of LC 3 II/I, ATG5, cle-Caspase-3, and Bax, as determined by a recovery experiment, the apoptosis rate was elevated, yet both P62 and Bcl-2 were significantly lower and LC3+ puncta per cells were significantly increased. Co-transfection of miR-153-3p-inhibition and sh-SNHG15 could reverse these results. Conclusion: LncRNA SNHG15 regulated autophagy and prevented from cerebral ischemia-reperfusion injury through mediating miR-153-3p/ATG5 axis.

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Section: Discussionsupporting

confidence: 91%

LncRNA SNHG15 regulates autophagy and prevents from cerebral ischemia-reperfusion injury through mediating miR-153-3p/ATG5 axis

Yu¹,

Cai²,

Zhou³

2023

Preprint

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“…This indicated that SNHG15 probably improve apoptosis through regulating autophagy. A previous study by Shen showed that knock‐out of SNHG15 could induce injury of N‐2a cells and inhibited apoptosis through inhibiting OGD, this was consistent with the present study 22 . The present study further detected autophagy and found that knock‐out of SNHG15 may improve apoptosis through inhibiting autophagy.…”

Section: Discussionsupporting

confidence: 91%

“…21 The present study constructed an in vitro ischaemia- this was consistent with the present study. 22 The present study further detected autophagy and found that knock-out of SNHG15 may improve apoptosis through inhibiting autophagy.…”

Section: Discussionmentioning

confidence: 55%

LncRNA SNHG15 regulates autophagy and prevents cerebral ischaemia‐reperfusion injury through mediating miR‐153‐3p/ATG5 axis

Yu,

Cai,

Zhou

2023

J Cellular Molecular Medi

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Ischaemic stroke is a common cerebrovascular disease. Long non‐coding RNA (lncRNA) of small nucleolar RNA host gene (SNHG15) has been supposedly performed a regulatory role in many diseases. Nonetheless, the function of SNHG15 in cerebral ischaemia‐reperfusion injury has not been clarified. The OGD/R of Neuro2A cells simulated the ischaemic and reperfused states of the brain. Neuro2a cell line with stable transfection of plasmid with silent expression of SNHG15 was constructed. Neuro2a cell lines transfected with miR‐153‐3p mimic (miR‐153‐3p‐mimics) and miR‐153‐3p inhibitor (miR‐153‐3p‐inhibition) were constructed. Expression of SNHG15, mi R‐200a, FOXO3 and ATG7 in mouse brain tissue and N2a cells was identified by qRT‐PCR. Western blot (WB) analysis of mouse brain tissue and Neuro2a cells revealed the presence of the proteins ATG5, Cle‐caspase‐3, Bax, Bcl‐2, LC3 II/I and P62 (WB). The representation and distribution of LC3B were observed by immunofluorescence. The death of cells was measured using a technique called flow cytometry (FACS). SNHG15 was highly expressed in cerebral ischaemia‐reperfusion injury model. Down‐regulation of SNHG15 lead to lower apoptosis rate and decreased autophagy. Dual luciferase assay and co‐immunoprecipitation (CoIP) found lncRNA SNHG15/miR‐153‐3p/ATG5. Compared to cells transfected with NC suppression, cells transfected with miR‐153‐3p‐inhibition had substantially greater overexpression of LC 3 II/I, ATG5, cle‐Caspase‐3, and Bax, as determined by a recovery experiment, the apoptosis rate was elevated, yet both P62 and Bcl‐2 were significantly lower and LC3+ puncta per cells were significantly increased. Co‐transfection of miR‐153‐3p‐inhibition and sh‐SNHG15 could reverse these results. LncRNA SNHG15 regulated autophagy and prevented cerebral ischaemia‐reperfusion injury through mediating the miR‐153‐3p/ATG5 axis.

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“… 37 Additionally, Chi et al found that miR-9 levels were decreased in the ischemic region of stroke model, and overexpression of miR-9 by miR-9 mimics attenuated ischemic stroke, 13 which was consistent with the previous study. 38–41 Our results revealed that miR-9-5p was down-regulated in the ipsilateral cortex of HI-injured mice, and overexpression of miR-9-5p could improve cerebral infarction, reduce brain edema and inhibit HI-induced apoptosis. These data suggested that up-regulated miR-9-5p expression might be an effective measure to alleviate brain injury caused by HI.…”

Section: Discussionmentioning

confidence: 56%

Up-Regulation of miR-9-5p Inhibits Hypoxia-Ischemia Brain Damage Through the DDIT4-Mediated Autophagy Pathways in Neonatal Mice

Gai¹,

Xing²,

Song³

et al. 2023

DDDT

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Introduction Hypoxia-ischemia (HI) remains the leading cause of cerebral palsy and long-term neurological sequelae in infants. Despite intensive research and many therapeutic approaches, there are limited neuroprotective strategies against HI insults. Herein, we reported that HI insult significantly down-regulated microRNA-9-5p (miR-9-5p) level in the ipsilateral cortex of neonatal mice. Methods The biological function and expression patterns of protein in the ischemic hemispheres were evaluated by qRT-PCR, Western Blotting analysis, Immunofluorescence and Immunohistochemistry. Open field test and Y-maze test were applied to detect locomotor activity and exploratory behavior and working memory. Results Overexpression of miR-9-5p effectively alleviated brain injury and improved neurological behaviors following HI insult, accompanying with suppressed neuroinflammation and apoptosis. MiR-9-5p directly bound to the 3’ untranslated region of DNA damage-inducible transcript 4 (DDIT4) and negatively regulated its expression. Furthermore, miR-9-5p mimics treatment down-regulated light chain 3 II/light chain 3 I (LC3 II/LC3 I) ratio and Beclin-1 expression and decreased LC3B accumulation in the ipsilateral cortex. Further analysis showed that DDIT4 knockdown conspicuously inhibited the HI-up-regulated LC3 II/ LC3 I ratio and Beclin-1 expression, associating with attenuated brain damage. Conclusion The study indicates that miR-9-5p-mediated HI injury is regulated by DDIT4-mediated autophagy pathway and up-regulation of miR-9-5p level may provide a potential therapeutic effect on HI brain damage.

show abstract

Knockdown of lncRNA SNHG15 Ameliorates Oxygen and Glucose Deprivation (OGD)-Induced Neuronal Injury via Regulating the miR-9-5p/TIPARP Axis

Cited by 6 publications

References 29 publications

LncRNA SNHG15 regulates autophagy and prevents from cerebral ischemia-reperfusion injury through mediating miR-153-3p/ATG5 axis

LncRNA SNHG15 regulates autophagy and prevents from cerebral ischemia-reperfusion injury through mediating miR-153-3p/ATG5 axis

LncRNA SNHG15 regulates autophagy and prevents cerebral ischaemia‐reperfusion injury through mediating miR‐153‐3p/ATG5 axis

Up-Regulation of miR-9-5p Inhibits Hypoxia-Ischemia Brain Damage Through the DDIT4-Mediated Autophagy Pathways in Neonatal Mice

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