Circular RNAs expression profiles and potential key molecules incompletely transected spinal cord injury.
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ABSTRACT:
PROVIDER: PRJNA659748 | ENA |
REPOSITORIES: ENA
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Project description:Circular RNA is implicated in numerous diseases and conditions, including traumatic injury to the central nervoussystem. However, we know little regarding their role in completely transected spinal cord injury (SCI). Our studyused high-throughput sequencing to analyze circular RNA expression in rats after experimental completetransection of spinal cord. We found differential expression in 400 circular RNAs after SCI, with 249 significantlyup-regulated and 151 significantly down-regulated. We then selected five circular RNAs for qRT-PCR validation,and the results were in agreement with RNA sequencing. Additionally, we predicted the function of circular RNAin SCI through GO and KEGG analyses, as well as the construction of circRNA/microRNA interaction networks.Furthermore, we identified circular RNA chr9:1829226-1834212 and mRNA Hdac11 as key molecules after SCI.In conclusion, this study is the first to characterize circular RNA function in rats after completely transected SCI,through identifying their differential expression. Our results provide insight into the mechanism and therapeutictargets of SCI.
2020-08-28 | GSE156999 | GEO
Project description:To determine whether the expression levels of circular RNAs were altered and lay a foundation for future work, we used high-throughput microarray analysis to screen circular RNAs expression patterns in the spinal cord of adult rats after traumatic spinal cord injury (SCI), finally to evaluate the potential rat models as a platform for the development of novel therapeutic targets for spinal cord injury in future clinical studies. Overall six rats at 3 days post-SCI in two groups were used to perform the microarray.
2018-05-15 | GSE114426 | GEO
Project description:Human astrocytes have reported to reprogram into neurons, but they have yet to be induced to three-dimensional (3D) neural tissue for neural organogenesis. Here, we demonstrate a remarkable strategy for 3D organoid generation by direct reprogramming human astrocytes. By combining overexpression OCT4, suppression p53 and small molecules CHIR99021, SB431542, RepSox and Y27632, termed as Op53-CSBRY, we successfully reprogramed human astrocytes into neural ectodermal cells and further induced human 3D-brain organoid. Those organoids can be finally induced into spinal cord organoids by activating FGF, SHH and BMP signaling. The grafts of Human astrocyte derived spinal cord organoids (hADSC-Organs) can survived, differentiated into spinal cord neurons, migrated long distance, formed synaptic connectivity with host neurons, bridged complete injury spinal cord tissue in mice. This method indicates that human astrocytes could be directly triggered neural organogenesis, and may hold a great promising to support local astrocytes in situ organogenesis after brain damages, such as stroke and spinal cord injury.
2024-02-01 | GSE168635 | GEO
Project description:Adult zebrafish have the ability to recover from spinal cord injury and exhibit re-growth of descending axons from the brainstem to the spinal cord. We performed gene expression analysis using microarray to find damage-induced genes after spinal cord injury, which shows that Sox11b mRNA is up-regulated at 11 days after injury. However, the functional relevance of Sox11b for regeneration is not known. Here, we report that the up-regulation of Sox11b mRNA after spinal cord injury is mainly localized in ependymal cells lining the central canal and in newly differentiating neuronal precursors or immature neurons. Using an in vivo morpholino-based gene knockout approach, we demonstrate that Sox11b is essential for locomotor recovery after spinal cord injury. In the injured spinal cord, expression of the neural stem cell associated gene, Nestin, and the proneural gene Ascl1a (Mash1a), which are involved in the self-renewal and cell fate specification of endogenous neural stem cells, respectively, is regulated by Sox11b. Our data indicate that Sox11b promotes neuronal determination of endogenous stem cells and regenerative neurogenesis after spinal cord injury in the adult zebrafish. Enhancing Sox11b expression to promote proliferation and neurogenic determination of endogenous neural stem cells after injury may be a promising strategy in restorative therapy after spinal cord injury in mammals. Spinal cord injury or control sham injury was performed on adult zebrafish. After 4, 12, or 264 hrs, a 5 mm segment of spinal cord was dissected and processed (as a pool from 5 animals) in three replicate groups for each time point and treatment.
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| PRJNA791374 | ENA
Project description:Adult zebrafish have the ability to recover from spinal cord injury and exhibit re-growth of descending axons from the brainstem to the spinal cord. We performed gene expression analysis using microarray to find damage-induced genes after spinal cord injury, which shows that Sox11b mRNA is up-regulated at 11 days after injury. However, the functional relevance of Sox11b for regeneration is not known. Here, we report that the up-regulation of Sox11b mRNA after spinal cord injury is mainly localized in ependymal cells lining the central canal and in newly differentiating neuronal precursors or immature neurons. Using an in vivo morpholino-based gene knockout approach, we demonstrate that Sox11b is essential for locomotor recovery after spinal cord injury. In the injured spinal cord, expression of the neural stem cell associated gene, Nestin, and the proneural gene Ascl1a (Mash1a), which are involved in the self-renewal and cell fate specification of endogenous neural stem cells, respectively, is regulated by Sox11b. Our data indicate that Sox11b promotes neuronal determination of endogenous stem cells and regenerative neurogenesis after spinal cord injury in the adult zebrafish. Enhancing Sox11b expression to promote proliferation and neurogenic determination of endogenous neural stem cells after injury may be a promising strategy in restorative therapy after spinal cord injury in mammals.
2010-10-19 | GSE20460 | GEO