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LncRNA DGCR5 suppresses neuronal apoptosis to improve acute spinal cord injury through targeting PRDM5.

ABSTRACT: Spinal cord injury (SCI) usually results in neurological damage. DGCR5 is closely related to neurological disorders, and this study aims to explore its role in neuronal apoptosis in acute SCI. The ASCI model was established in rats, and the Basso, Beattie, and Bresnahan (BBB) scoring was used to assess the neurological function. The expression of RNA and protein was quantified by quantitative real-time PCR (qRT-PCR) and western blotting, respectively. The oxygenglucose deprivation (OGD) was performed upon neurons and apoptosis was evaluated by flow cytometry. The interaction and binding between DGCR5 and PRDM5 was detected with RNA pull-down and RIP assay, respectively. DGCR5 was down-regulated in ASCI model rat and in neurons treated with hypoxia. Over-expression of DGCR5 inhibited neuronal apoptosis. Interaction between DGCR5 negatively regulated PRDM5 protein expression by binding and interacting with it. DGCR5 inhibited neuronal apoptosis through PRDM5. Over-expressed DGCR5 ameliorated ASCI in rat. DGCR5 suppresses neuronal apoptosis through directly binding and negatively regulating PRDM5, and thereby ameliorating ASCI.

SUBMITTER: Zhang H

PROVIDER: S-EPMC6224267 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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LncRNA DGCR5 suppresses neuronal apoptosis to improve acute spinal cord injury through targeting PRDM5.

Zhang Huafeng H Wang Wengang W Li Ning N Li Peng P Liu Ming M Pan Junwei J Wang Dan D Li Junwei J Xiong Yuanyuan Y Xia Lei L

Cell cycle (Georgetown, Tex.) 20180911 16

Spinal cord injury (SCI) usually results in neurological damage. DGCR5 is closely related to neurological disorders, and this study aims to explore its role in neuronal apoptosis in acute SCI. The ASCI model was established in rats, and the Basso, Beattie, and Bresnahan (BBB) scoring was used to assess the neurological function. The expression of RNA and protein was quantified by quantitative real-time PCR (qRT-PCR) and western blotting, respectively. The oxygenglucose deprivation (OGD) was perf ...[more]

PMID: 30146926

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Project description:BackgroundSpinal cord injury (SCI) is a neurological disease associated with a high disability rate. Low-dose lipopolysaccharide (LPS) has been reported to activate cross-immune tolerance and alleviate the effects of various traumatic stimuli. The present study aimed to explore the effect of LPS on SCI and the potential molecular mechanism.MethodsMale Sprague-Dawley (SD) rats were used to established an in vivo SCI model and were intraperitoneally injected with lentivirus particles encoding a MALAT1 small interfering RNA (siRNA) on day 10 prior to SCI and with 0.2 mg/kg LPS 72 h prior to SCI. Basso, Beattie, and Bresnahan (BBB) scoring; HE staining; and TUNEL assay were used to assess neurological function and pathophysiological changes. Western blot and immunohistochemistry (IHC) were used to detect cell autophagy and Nrf2 nuclear translocation. PC12 cells were exposed to oxygen-glucose deprivation/reoxygenation (OGD/R) to establish an in vitro SCI model. In vitro SCI model cells were pretreated with LPS and transfected with siMALAT1 or MALAT1 overexpression plasmid aimed at knocking down MALAT1 or overexpressing MALAT1. The cell counting kit-8 (CCK-8) assay was used to measure the toxicity of LPS towards PC12 cells. Flow cytometry and immunofluorescence analysis were performed to investigate cell apoptosis and Nrf2 nuclear translocation.ResultsSCI rats preconditioned with low-dose LPS had higher BBB scores, reduced SCI injury, increased MALAT1 expression and activated autophagy and Nrf2 nuclear translocation in the in vivo SCI model. In the in vitro SCI model, low-dose LPS treatment suppressed the apoptotic ratio of PC12 cells, increased MALAT1 expression, activated autophagy, and promoted Nrf2 nuclear translocation. Silencing MALAT1 exacerbated OGD/R injury in vitro and weakened the protective effect of low-dose LPS. Overexpression of MALAT1 inhibits OGD/R-induced apoptosis by inducing autophagy and promoting Nrf2 nuclear translocation. This was also been confirmed in animal experiments, silencing MALAT1 blocked the promotion of Nrf2 by low-dose LPS and the alleviated of SCI apoptosis.ConclusionsLow-dose LPS exhibited a protective role on SCI by activating autophagy and suppressing nerve cell apoptosis via the lncRNA MALAT1/Nrf2 axis.

Project description:BackgroundThere is emerging evidence that astaxanthin plays a significant role in protecting neuro-cells from apoptosis after central nervous system injury. Our study examined the effects of astaxanthin on neuro-cell apoptosis after spinal cord injury.MethodsOne hundred and forty-four healthy adult Sprague-Dawley rats were randomly divided into the experimental group, control group, and sham operation group (n=48). Spinal cord injury was induced using the modified Allen method in the control group and the experimental group; while in the sham operation group, the lamina was removed without spinal cord injury. The rats in the experimental group were given astaxanthin (75 mg/kg) by gavage immediately after the operation, and in the other groups were given the same amount of olive oil. Motor function was assessed by blood-brain barrier (BBB) scores. The malondialdehyde (MDA) content and the activity of superoxide dismutase (SOD) at 24 h was determined after the operation. The apoptosis index (AI) was determined at 6, 24, and 48 h after the operation. At 48 h after the operation, we calculated the water content of the spinal cord, the lesion ratio of the spinal cord, the ultrastructure of the spinal cord, and the ultrastructure score.ResultsThe BBB scores of the control and experimental groups were significantly lower than the sham operation group at each postoperative time (P<0.05), and the BBB score of the experimental group was significantly higher than the control group at 1-4 weeks postoperatively (P<0.05). At 24 hours postoperatively, MDA content was highest in the control group and lowest in the sham operation group, while SOD activity was highest in the sham operation group and lowest in the control group (P<0.05). At each time point postoperatively, the sham operation group had the lowest AI and the control group had the highest AI (P<0.05). At 48 h after the operation, the water content and the lesion ratio of the spinal cord, and the ultrastructure score were the lowest in the sham operation group and the highest in the control group (P<0.05).ConclusionsAstaxanthin significantly improved the motor function of rats with spinal cord injury.

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LncRNA DGCR5 suppresses neuronal apoptosis to improve acute spinal cord injury through targeting PRDM5.

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LncRNA DGCR5 suppresses neuronal apoptosis to improve acute spinal cord injury through targeting PRDM5.

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