Knockdown of Nogo gene by short hairpin RNA interference promotes functional recovery of spinal cord injury in a rat model

Liu, Guomin; Luo, Yungang; Li, Juan; Xu, Kun

doi:10.3892/mmr.2016.5072

Cited by 12 publications

(5 citation statements)

References 36 publications

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“…It is generally accepted that C-terminal region (Nogo-66) of Nogo-A transduces the inhibitory signal into the cell interior of neurons by combining with Nogo-66 receptor (NgR). The research reports that treatment with Nogo shRNAs, which can knockdown Nogo gene expression, improved function recovery of spinal cord injury rats [37]. In the present study, we found that PF treatment suppressed Nogo-A expression in the injured spinal cord.…”

Section: Discussionsupporting

confidence: 69%

Neuroprotection by Paeoniflorin against Nuclear Factor Kappa B-Induced Neuroinflammation on Spinal Cord Injury

Wang

Dai

Shi

et al. 2018

BioMed Research International

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Background Acute spinal cord injury (SCI) is one of the most common and devastating causes of sensory or motor dysfunction. Nuclear factor-kappa B(NF-κB)-mediated neuroinflammatory responses, in addition to nitric oxide (NO), are key regulatory pathways in SCI. Paeoniflorin (PF), a major active component extracted from Paeonia roots, has been suggested to exert neuroprotective effects in the central nervous system. However, whether PF could improve the motor function after SCI in vivo is still unclear. Method Immunohistochemical analysis, western blot, real-time quantitative PCR, immunofluorescence staining, and histopathological and behavioral evaluation were used to explore the effects of paeoniflorin after SCI for 14 days. Results In this study, PF treatment significantly inhibited NF-κB activation and downregulated the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2(COX-2), and Nogo-A. Comparing behavioral and histological changes in SCI and PF treatment groups, we found that PF treatment improved motor function recovery, attenuated the histopathological damage, and increased neuronal survival in the SCI model. PF treatment also reduced expression levels of Bax and c-caspase-3 and increased the expression level of Bcl-2 and cell viabilities. Upregulation of TNF-α, IL-6, and IL-1β after injury was also prevented by PF. Conclusion These results suggest that the neuroprotective effects of PF are related to the inhibition of the NF-κB signaling pathway. And PF may be a therapeutic strategy in spinal cord injury.

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Section: Discussionsupporting

confidence: 69%

Neuroprotection by Paeoniflorin against Nuclear Factor Kappa B-Induced Neuroinflammation on Spinal Cord Injury

Wang

Dai

Shi

et al. 2018

BioMed Research International

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“…GAP-43 protein used for the labeling of axonal growth is mainly expressed at the regenerated axonal terminal [18][19][20]. Previously, up-regulation of GAP-43 was associated with the motor function recovery in both brain and spinal cord injury animal models [21][22][23]. In our study, the motor function recovery can be observed in the model group.…”

Section: Discussionsupporting

confidence: 57%

Expression of Slit and Robo during remodeling of corticospinal tract in cervical spinal cord in middle cerebral artery occlusion rats

Ying

Jiang³

et al. 2021

Mol Biol Rep

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Background: Slits and Robos were associated with the generation of axons of corticospinal tract during the corticospinal tract (CST) remodeling after the cerebral ischemic stroke (CIS). However, little is known about the mechanism of CST remodeling. In this study, we detected the expression of Slits and Robos in middle cerebral artery occlusion (MCAO) rats to investigate the roles of Slits and Robos in the CIS. Methods: MCAO model was established using modi ed Zea Longa method. Beam walking test (BWT) was conducted to evaluate the motor function. The images of the track of cortical spinal cord beam on day 7, 14 and 21 were observed by anterograde CST tracing. Biopinylated dextan amine (BDA) was used to mark CST anterogradely. Expression of GAP-43 mRNA and GAP-43 protein in cervical spinal cord was detected by Real-Time PCR and Western blot analysis, respectively. The expression of Slit1, Slit2 and Robo1 in cervical spinal cord was detected by immuno uorescence staining.Results: The scores in the model group were signi cantly reduced compared to sham-operation group on day 7 (P<0.001), 14 (P<0.001) and 21 (P<0.001), respectively. There was no signi cant difference in the score on day 7, 14 and 21 of the sham-operation groups (P>0.05). In contrast, signi cant increase was noticed in the scores in model group, presenting a time-dependent manner. More CST staining bers could be observed at the degenerative side in the model group compared with that of the sham-operation group on day 21. GAP-43 mRNA expression in the model group showed signi cant increase compared to that of sham-operation group on day 14 (P=0.015) and 21 days (P=0.002). The expression of GAP-43 protein in model group showed signi cant increase compared to that of sham-operation group on day 14 (P=0.022) and day 21 (P=0.008), respectively. The expression of Slit1 and Slit2 showed increase on day 14 and day 21, while the expression of Robo1 showed signi cant decrease in MCAO rats.

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“…In primary retinal ganglion cells, Nogo-A RNA inhibition or a peptide antagonist of the Nogo-66 functional domain promoted axonal outgrowth as assessed using GAP-43 immunofluorescence (Huo et al, 2013 ) suggesting a close relationship between GAP-43 and neurite extension induced by inhibition of Nogo-A function. In rats with spinal cord hemisection, adenovirus-mediated transfection of Nogo-A short hairpin RNAs were found to reduce the expression of the Nogo-A gene and upregulate GAP-43 expression with an associated functional recovery of the injured nerves (Liu et al, 2016 ). Therefore, impeding Nogo gene expression may be an important step leading to the upregulation of GAP-43 in the promotion of spinal cord axonal outgrowth.…”

Section: Gap-43 As a Mediator Of Axonal Outgrowthmentioning

confidence: 99%

A Shift from a Pivotal to Supporting Role for the Growth-Associated Protein (GAP-43) in the Coordination of Axonal Structural and Functional Plasticity

Holahan

2017

Front. Cell. Neurosci.

132

100

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In a number of animal species, the growth-associated protein (GAP), GAP-43 (aka: F1, neuromodulin, B-50, G50, pp46), has been implicated in the regulation of presynaptic vesicular function and axonal growth and plasticity via its own biochemical properties and interactions with a number of other presynaptic proteins. Changes in the expression of GAP-43 mRNA or distribution of the protein coincide with axonal outgrowth as a consequence of neuronal damage and presynaptic rearrangement that would occur following instances of elevated patterned neural activity including memory formation and development. While functional enhancement in GAP-43 mRNA and/or protein activity has historically been hypothesized as a central mediator of axonal neuroplastic and regenerative responses in the central nervous system, it does not appear to be the crucial substrate sufficient for driving these responses. This review explores the historical discovery of GAP-43 (and associated monikers), its transcriptional, post-transcriptional and post-translational regulation and current understanding of protein interactions and regulation with respect to its role in axonal function. While GAP-43 itself appears to have moved from a pivotal to a supporting factor, there is no doubt that investigations into its functions have provided a clearer understanding of the biochemical underpinnings of axonal plasticity.

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Knockdown of Nogo gene by short hairpin RNA interference promotes functional recovery of spinal cord injury in a rat model

Cited by 12 publications

References 36 publications

Neuroprotection by Paeoniflorin against Nuclear Factor Kappa B-Induced Neuroinflammation on Spinal Cord Injury

Neuroprotection by Paeoniflorin against Nuclear Factor Kappa B-Induced Neuroinflammation on Spinal Cord Injury

Expression of Slit and Robo during remodeling of corticospinal tract in cervical spinal cord in middle cerebral artery occlusion rats

A Shift from a Pivotal to Supporting Role for the Growth-Associated Protein (GAP-43) in the Coordination of Axonal Structural and Functional Plasticity

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