CircRNA_01477 influences axonal growth via regulating miR-3075/FosB/Stat3 axis

Qian, Xiaowei; Lin, Ge; Wang, Junpei; Zhang, Siming; Ma, Jingyi; Yu, Bin; Wu, Ronghua; Liu, Yan

doi:10.1016/j.expneurol.2021.113905

Cited by 15 publications

(13 citation statements)

References 29 publications

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“…The time schedule and schematic diagram of the SCI sites and SASH1 siRNA (siSASH1) injection sites are shown in Figure 1Ba–b. For the in vivo siRNA treatment, we injected methoxy‐modified siSASH1 to allow siRNA knockdown for a longer duration in accordance with our previous study 20 . We detected the efficiency of siSASH1, and the results showed (Figure 1Ca–b) that SASH1 protein decreased to 74% and 51% at 7 and 14 days post‐injury, respectively, compared with the control siRNA (siCtrl) group.…”

Section: Resultsmentioning

confidence: 55%

“…For the in vivo siRNA treatment, we injected methoxy‐modified siSASH1 to allow siRNA knockdown for a longer duration in accordance with our previous study. 20 We detected the efficiency of siSASH1, and the results showed (Figure 1Ca–b ) that SASH1 protein decreased to 74% and 51% at 7 and 14 days post‐injury, respectively, compared with the control siRNA (siCtrl) group. Considering that siRNA efficiency tends to fade after 2 weeks, we collected the data until 3 weeks after SCI.…”

Section: Resultsmentioning

confidence: 97%

“…Immunofluorescence (IF) assays were performed as described previously. 16 , 17 , 20 Cultured neurons were fixed with 4% paraformaldehyde for 30 minutes. Then the cultures were washed with phosphate‐buffered saline (PBS) three times and blocked for 60 minutes.…”

Section: Methodsmentioning

confidence: 99%

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Depletion of SASH1, an astrocyte differentiation‐related gene, contributes to functional recovery in spinal cord injury

et al. 2022

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Aims This study aimed to evaluate the effects of the depletion of SAM and SH3 domain‐containing protein 1 (SASH1) on functional recovery after spinal cord injury (SCI) and to investigate the possible mechanism of SASH1 knockdown in astrocytes facilitating axonal growth. Methods SCI model was established in adult rats. SASH1 small interfering RNA (siSASH1) was used to investigate its function. Hindlimb motor function was evaluated by the Basso‐Bresnahan‐Beattie (BBB) assay. The gene expressions were evaluated by the methods of qRT‐PCR, Western‐blotting, ELISA, and immunohistochemistry. Results SASH1 knockdown improved the BBB scores after SCI and significantly reduced GFAP expression. In cultured spinal astrocytes, siSASH1 treatment decreased interferon‐γ release and increased brain‐derived neurotrophic factor (BDNF) release. When cocultured with SASH1‐knockdown astrocytes, axonal growth increased. The neuronal tropomyosin receptor kinase B (BDNF receptor) expression increased, especially in the axonal tips. SASH1 expression increased while NSCs differentiated into glial cells, instead of neurons. After SASH1 depletion, differentiated NSCs maintained a higher level of Nestin protein and an increase in BDNF release. Conclusions These results indicate that SASH1 acts as an astrocytic differentiation‐maintaining protein, and SASH1 downregulation limits glial activation and contributes toward functional recovery after SCI.

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Section: Resultsmentioning

confidence: 55%

Section: Resultsmentioning

confidence: 97%

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Depletion of SASH1, an astrocyte differentiation‐related gene, contributes to functional recovery in spinal cord injury

et al. 2022

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“…Again, we looked up in the CCALD database for clues, for brains from children are still developing. We focused on genes related to the main signaling pathways governing nervous system development at several stages and anatomical levels, including neuronal maturation, morphogenesis of dendritic arbors, axon guidance and synaptogenesis: Wnt 51 , Notch 52 , Sonic hedgehog ( Shh ) 53 , neurotrophins 53 , Stat3 54,55 .…”

Section: Resultsmentioning

confidence: 99%

Defective neuritogenesis inAbcd1/2deficient rat neurons due to intrinsic and astrocyte-dependent mechanisms

Golbano

Pardo

Menacho-Pando

et al. 2022

Preprint

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X-linked adrenoleukodystrophy (X-ALD) is a rare neurometabolic and demyelinating disorder caused by loss of function mutations of the ABCD1 transporter that imports very-long-chain fatty acids (VLCFA) into the peroxisome for beta-oxidation. Impaired ABCD1 function results in VLCFA accumulation, which ultimately causes lethal forms of X-ALD in children (CCALD) and adults (CAMN). Because X-ALD is a genetic disorder, we looked for signs of altered neurodevelopmental pathways in the transcriptomes of brain cortical tissues free of pathology from patients that died of CALD or CAMN. Several categories related to brain development, axonal growth, synaptic signaling and synaptic compartments were significantly dysregulated in both CALD and CAMN, suggesting that congenital circuit abnormalities might be structural in brains of mutated ABCD1 carriers. We partially dissected the cellular origin of dysregulated pathways using rat neuronal and astrocytic cultures in which X-ALD was modeled by silencing of Abcd1 and Abcd2 by RNA interference. Abcd2 was silenced lest it compensated for Abcd1 loss. Abcd1/2 deficient neurons presented higher rates of death, reduced sizes and defective formation of spines, dendrites and axons. The aberrant neuron development was caused by cell-autonomous and astrocyte-dependent mechanisms, and involved Wnt signaling, as suggested by the rescue of the expression of a synaptic gene upon pharmacological activation of the Wnt pathway. As recently proposed for neurogenetic disorders such as Huntington's disease, our data suggest that X-ALD has a neurodevelopmental component that may cause psychiatric alterations and prime neural circuits for neurodegeneration. If this is the case, therapies aimed at restoring neural-circuit function in neurodevelopmental disorders may be reprofiled for X-ALD therapeutics.

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“…The hippocampus has been shown to express specific regions of circRNAs in the mouse brain (Rybak-Wolf et al, 2015). Some studies have shown that circRNAs are specifically located in dendrite (You et al, 2015), axons (Qian et al, 2022) and synapses (Curry-Hyde et al, 2020), regulating synaptic plasticity (Xu et al, 2020). CircRNAs also play a causative role in aging and longevity, whose levels are also altered in an age-dependent manner across specific human organs and tissues (Kim et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice

Wang

Gao

et al. 2022

Front. Mol. Neurosci.

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IntroductionAge is an established risk factor for neurodegenerative disorders. Aging-related cognitive decline is a common cause of memory impairment in aging individuals, in which hippocampal synaptic plasticity and hippocampus-dependent memory formation are damaged. Circular RNAs (circRNAs) have been reported in many cognitive disorders, but their role in aging-related memory impairment is unclear.Methods: In this study, we aimed to investigate the effects of circ-Vps41 on aging-related hippocampus-dependent memory impairment and explore the potential mechanisms. Here, D-galactose was used to produce a conventional aging model resulting in memory dysfunction.ResultsCirc-Vps41 was significantly downregulated in D-galactose-induced aging in vitro and in vivo. The overexpression of circ-Vps41 could upregulate synaptophysin (Syp), thereby promoting the synaptic plasticity and alleviating cognitive impairment in aging mice. Mechanistically, we found that circ-Vps41 upregulated Syp expression by physically binding to miR-24-3p. Moreover, the miR-24-3p mimics reversed the circ-Vps41 overexpression-induced increase in Syp expression.DiscussionOverexpression of circ-Vps41 alleviated the synaptic plasticity and memory dysfunction via the miR-24-3p/Syp axis. These findings revealed circ-Vps41 regulatory network and provided new insights into its potential mechanisms for improving aging-related learning and memory impairment.

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CircRNA_01477 influences axonal growth via regulating miR-3075/FosB/Stat3 axis

Cited by 15 publications

References 29 publications

Depletion of SASH1, an astrocyte differentiation‐related gene, contributes to functional recovery in spinal cord injury

Depletion of SASH1, an astrocyte differentiation‐related gene, contributes to functional recovery in spinal cord injury

Defective neuritogenesis inAbcd1/2deficient rat neurons due to intrinsic and astrocyte-dependent mechanisms

Circ-Vps41 positively modulates Syp and its overexpression improves memory ability in aging mice

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