Antisense vimentin cDNA combined with chondroitinase ABC promotes axon regeneration and functional recovery following spinal cord injury in rats

Xia, Yongzhi; Yan, Yuying; Xia, Haijian; Zhao, Tianzhi; Chu, Weihua; Hu, S. Jack; Feng, Hua; Lin, Jiangkai

doi:10.1016/j.neulet.2015.01.073

Cited by 13 publications

(5 citation statements)

References 20 publications

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“…Hence, exploring novel strategies for SCI has sparked great interest for researchers. Our past studies have uncovered a variety of therapeutic candidates associated with secondary injury, including promoting neuron survival through inhibiting acid-sensing ion channel 1a (ASIC 1a) [4] or activating G-protein coupled estrogen receptor 1 (GPER1) [2,5], mediating neuroin ammation by complement C5a [6], decreasing glial scar formation and potentiating axon regeneration using curcumin, antisense vimentin cDNA combined with chondroitinase ABC [7][8][9], and cell-based strategies using exogenous transplantation of human umbilical cord mesenchymal stem cells [10] and directing endogenous neural stem cells (NSCs) differentiation into neurons [11,12]. However, majority of SCI patients still recover poorly in clinic, implying that more mechanisms need to be elucidated with respect to secondary injury, and exploring more effective treatment for SCI is of great signi cance.…”

Section: Introductionmentioning

confidence: 99%

Ferrostatin-1 Alleviates White Matter Injury Via Decreasing Ferroptosis Following Spinal Cord Injury

Xue

Xian

et al. 2021

Mol Neurobiol

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Spinal cord injury (SCI), a devastating neurological impairment, ubiquitously imposes a long-term psychological stress and high socioeconomic burden for the suffers and their family. To date, recent researchers have paid arousing attention to white matter injury and uncovering the underlying mechanism post-SCI. Ferroptosis, to our knowledge, has been revealed to be associated with diverse diseases including stroke, cancer, and kidney degeneration. However, its role in white matter damage after SCI remains unclear. Ferrostatin-1, a potent inhibitor of ferroptosis, has been illustrated to curb ferroptosis in neurons, subsequently improve functional recovery after traumatic brain injury (TBI). But whether it inhibits white matter injury post-SCI is still unknown. Here, our results indicated that ferroptosis played an important role in the secondary white matter injury following SCI and ferrostatin-1 could reduce iron and reactive oxygen species (ROS) accumulation, downregulate the ferroptosis-related genes and its products of IREB2 and PTGS2 to further inhibit ferroptosis in oligodendrocyte progenitor cells (OPCs), nally reducing white matter injury and promoting functional recovery following SCI in rats, which enlarges the therapeutic scope for ferrostatin-1 and deciphers the potential mechanism of white matter damage after SCI.

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Section: Introductionmentioning

confidence: 99%

Ferrostatin-1 Alleviates White Matter Injury Via Decreasing Ferroptosis Following Spinal Cord Injury

Xue

Xian

et al. 2021

Mol Neurobiol

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“…The search resulted in 1,096 non-duplicate articles. After studying the titles and abstracts of these articles, 136 articles were regarded as potentially eligible to enter this review, and finally, 34 articles were included ( Bai et al, 2010 ; Bradbury et al, 2002 ; Caggiano et al, 2005 ; Cheng et al, 2015 ; Führmann et al, 2018 ; García-Alías et al, 2009 ; García-Alías et al, 2008 ; García-Alías et al, 2011 ; Grosso et al, 2014 ; Huang et al, 2006 ; Ishikawa et al, 2015 ; Janzadeh et al, 2017 ; Karimi-Abdolrezaee et al, 2010 ; Kim et al, 2006 ; Lee et al, 2012 ; Liu, et al, 2018 ; Mountney et al, 2013 ; Ni et al, 2015 ; Novotna et al, 2018; Raspa, Bolla et al, 2019 ; Sarveazad et al, 2017 ; Sarveazad et al, 2014 ; Shinozaki et al, 2016 ; Takeuchi et al, 2013 ; Tom et al, 2009 ; Wang et al, 2011a ; Wang et al, 2011b ; Xia et al, 2017 ; Xia et al, 2015 ; Xiong et al, 2016 ; Yang et al, 2009 ; Yoo et al, 2013 ; Zhao et al, 2013 ) ( Figure 1 ). These 34 studies contained 44 separate experiments evaluating several different protocols, including variations in the SCI severity, the prescription method, the prescription dose, and the interval time between SCI and ChABC administration.…”

Section: Resultsmentioning

confidence: 99%

Chondroitinase ABC Administration in Locomotion Recovery After Spinal Cord Injury: A Systematic Review and Meta-analysis

Yousefifard

Janzadeh

Ali

et al. 2022

BCN

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Objective: The present systematic review and meta-analysis intends to conduct a comprehensive and complete search in electronic resources to investigate the role of administrating ChABC in improving complications following SCI. Methods: Medline, Embase, Scopus and Web of sciences were searched until the end of 2019. Two independent reviewers assessed the studies conducted on rats and mice and summarized the data. Using STATA 14.0 program, the findings were reported as pooled standardized mean differences (SMD) with 95% confidence intervals (CI). Results: 34 pre-clinical studies were included. ChABC administration generally improves locomotion recovery after SCI (SMD = 0.90; 95% CI: 0.61 to 1.20; p <0.001). Subgroup analysis showed that differences in SCI model (p = 0.732), severity of injury (p = 0.821), number of ChABC administration (p = 0.092), blinding status (p = 0.294), use of different locomotor score (p = 0.567) and follow up duration (p = 0.750) have no effect on the efficacy of ChABC treatment. Conclusion: The findings of the present study showed that prescribing ChABC has a moderate effect in the improvement of locomotion after SCI in mice and rats. However, this moderate effect introduces ChABC as an adjuvant therapy and not as a primary therapy.

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“…When this was combined with ChABC, it reduced glial scar and cystic cavity formation after SCI in rats ( Xia et al, 2008 ). In a follow-up report, the investigators found that this combined treatment promoted axon regeneration and functional recovery after SCI, indicating that axon regeneration may be promoted by modified physical and biochemical characteristics of intra- and extracellular architecture in glial scar tissues ( Xia et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

Combined RhoA morpholino and ChABC treatment protects identified lamprey neurons from retrograde apoptosis after spinal cord injury

Hu,

Zhang,

Rodemer

et al. 2023

Front. Cell. Neurosci.

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Previously, we reported that RhoA knockdown by morpholino antisense oligonucleotides (MOs), and enzymatic digestion of chondroitin sulfate proteoglycans (CSPGs) at the site of injury with chondroitinase ABC (ChABC), each can reduce retrograde neuronal apoptosis after spinal cord transection in the lamprey. To elucidate the mechanisms in neuronal survival and axon regeneration, we have investigated whether these two effects are additive in vivo. We used lampreys as a spinal cord injury model. MOs were used to knockdown RhoA and Chondroitinase ABC (ChABC) was used to digest CSPGs in vivo. Retrograde labeling, fluorochrome-labeled inhibitor of caspase activity (FLICA), immunohistochemistry, and western blots were performed to assess axonal regeneration, neuronal apoptotic signaling and Akt activation. Four treatment combinations were evaluated at 2-, 4-, and 10-weeks post-transection: (1) Control MO plus enzyme buffer (Ctrl); (2) control MO plus ChABC; (3) RhoA MO plus enzyme buffer (RhoA MO); and (4) RhoA MO plus ChABC (RhoA MO + ChABC). Consistent with our previous findings, at 4-weeks post-transection, there was less caspase activation in the ChABC and RhoA MO groups than in the Ctrl group. Moreover, the RhoA MO plus ChABC group had the best protective effect on identified reticulospinal (RS) neurons among the four treatment combinations. At 2 weeks post-transection, when axons have retracted maximally in the rostral stump and are beginning to regenerate back toward the lesion, the axon tips in the three treatment groups each were closer to the transection than those in the Ctr MO plus enzyme buffer group. Long-term axon regeneration also was evaluated for the large, individually identified RS neurons at 10 weeks post-transection by retrograde labeling. The percent regenerated axons in the RhoA MO plus ChABC group was greater than that in any of the other groups. Akt phosphorylation levels at threonine 308 was quantified in the identified RS neurons by western blots and immunofluorescence. The RhoA MO plus ChABC treatment enhanced pAkt-308 phosphorylation more than any of the other treatment groups. Although some of the effects of CSPGs are mediated through RhoA activation, some growth-inhibiting mechanisms of RhoA and CSPGs are independent of each other, so combinatorial therapies may be warranted.

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Antisense vimentin cDNA combined with chondroitinase ABC promotes axon regeneration and functional recovery following spinal cord injury in rats

Cited by 13 publications

References 20 publications

Ferrostatin-1 Alleviates White Matter Injury Via Decreasing Ferroptosis Following Spinal Cord Injury

Ferrostatin-1 Alleviates White Matter Injury Via Decreasing Ferroptosis Following Spinal Cord Injury

Chondroitinase ABC Administration in Locomotion Recovery After Spinal Cord Injury: A Systematic Review and Meta-analysis

Combined RhoA morpholino and ChABC treatment protects identified lamprey neurons from retrograde apoptosis after spinal cord injury

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