Expression of CDc6 after acute spinal cord injury in adult rats

Chen, Chen; Lu, Jian; Yu, Qin; Xiao, Jianru; Wei, Haifeng; Song, Xinjian; Ge, Jianbing; Tao, Weidong; Qian, Rong; Yu, Xiaowei; Zhao, Jian

doi:10.1016/j.npep.2016.02.002

Cited by 4 publications

(1 citation statement)

References 41 publications

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“…One other key HR protein, breast cancer gene 1 (BRCA1), has likewise been reported to be more highly expressed in microglia of SCI groups using RNA sequencing [ 79 ]. Proliferating cell nuclear antigen (PCNA), a central replication factor and an auxiliary protein to several DNA repair pathways, has been reported to be upregulated in three independent studies [ 80 , 81 , 82 ]. The DNArep protein mini-chromosome maintenance complex component 7 (MCM7), the FA-related Fanconi anemia complementation group D2 (FANCD2), and ataxia-telangiectasia and rad3-related (ATR) were found to be upregulated as well [ 49 , 79 , 81 ].…”

Section: The Dna Damage Response Is Understudied In Scimentioning

confidence: 99%

Oxidative DNA Damage in the Pathophysiology of Spinal Cord Injury: Seems Obvious, but Where Is the Evidence?

2022

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Oxidative stress occurs at various phases of spinal cord injury (SCI), promoting detrimental processes such as free radical injury of proteins, nucleic acids, lipids, cytoskeleton, and organelles. Oxidative DNA damage is likely a major contributor to the pathogenesis of SCI, as a damaged genome cannot be simply turned over to avert detrimental molecular and cellular outcomes, most notably cell death. Surprisingly, the evidence to support this hypothesis is limited. There is some evidence that oxidative DNA damage is increased following SCI, mainly using comet assays and immunohistochemistry. However, there is great variability in the timing and magnitude of its appearance, likely due to differences in experimental models, measurement techniques, and the rigor of the approach. Evidence indicates that 8-oxodG is most abundant at 1 and 7 days post-injury (dpi), while DNA strand breaks peak at 7 and 28 dpi. The DNA damage response seems to be characterized by upregulation of PCNA and PARP1 but downregulation of APEX1. Significant improvements in the analysis of oxidative DNA damage and repair after SCI, including single-cell analysis at time points representative for each phase post-injury using new methodologies and better reporting, will uncover the role of DNA damage and repair in SCI.

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Section: The Dna Damage Response Is Understudied In Scimentioning

confidence: 99%

Oxidative DNA Damage in the Pathophysiology of Spinal Cord Injury: Seems Obvious, but Where Is the Evidence?

2022

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Effect of CLIP3 Upregulation on Astrocyte Proliferation and Subsequent Glial Scar Formation in the Rat Spinal Cord via STAT3 Pathway After Injury

Chen

Hao

et al. 2017

J Mol Neurosci

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Spinal cord injury (SCI) is a devastating event resulting in neuron degeneration and permanent paralysis through inflammatory cytokine overproduction and glial scar formation. Presently, the endogenous molecular mechanisms coordinating glial scar formation in the injured spinal cord remain elusive. Signal transducer and activator of transcription 3 (STAT3) is a well-known transcription factor particularly involving in cell proliferation and inflammation in the lesion site following SCI. Meanwhile, CAP-Gly domain containing linker protein 3(CLIP3), a vital cytoplasmic protein, has been confirmed to providing an optimal conduit for intracellular signal transduction and interacting with STAT3 with mass spectrometry analysis. In this study, we aimed to identify the expression of CLIP3 in the spinal cord as well as its role in mediating astrocyte activation and glial scar formation after SCI by establishing an acute traumatic SCI model in male adult rats. Western blot analysis revealed that CLIP3 increased gradually after injury, reached a peak at day 3. The immunohistochemistry staining showed the same result in white matter. With double immunofluorescence staining, we found that CLIP3 was expressed in glial cells and significant changes of CLIP3 expression occurred in astrocytes during the pathological process. Statistical analysis demonstrated there was a correlation between the number of positive cells stained by CLIP3 and STAT3 in the spinal cord after SCI. Co-immunoprecipitation further indicated that CLIP3 interacted with STAT3 in the injured spinal cord. Taken together, our study clearly suggested that CLIP3 played an essential role in astrocyte activation, associating with the STAT3 pathway activation induced by SCI.

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Downregulation of Cdc6 inhibits tumorigenesis of osteosarcoma in vivo and in vitro

Jiang

Liu

et al. 2019

Biomedicine & Pharmacotherapy

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Expression of CDc6 after acute spinal cord injury in adult rats

Cited by 4 publications

References 41 publications

Oxidative DNA Damage in the Pathophysiology of Spinal Cord Injury: Seems Obvious, but Where Is the Evidence?

Oxidative DNA Damage in the Pathophysiology of Spinal Cord Injury: Seems Obvious, but Where Is the Evidence?

Effect of CLIP3 Upregulation on Astrocyte Proliferation and Subsequent Glial Scar Formation in the Rat Spinal Cord via STAT3 Pathway After Injury

Downregulation of Cdc6 inhibits tumorigenesis of osteosarcoma in vivo and in vitro

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