Time representation of mitochondrial morphology and function after acute spinal cord injury

Jia, Zhiqiang; Li, Gang; Zhang, Zhenyu; Li, Hao-tian; Wang, Jiquan; Fan, Zhongkai; Lv, Gang

doi:10.4103/1673-5374.175061

Cited by 31 publications

(5 citation statements)

References 40 publications

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“…As shown in Figure 2 , the treatment of ICA increased GSH and SOD, but decreased the level of MDA at 24 h and 3 days after SCI. This is consistent with our previous research on the time-dependent mitochondrial function and morphology in SCI ( Jia et al, 2016 ). What important is that, although there is no statistical difference between ICA 20 μmol/kg group and 50 μmol/kg group at 24 h after SCI, the mice treated with 50 μmol/kg ICA exhibited a significant reduction in MDA but increase in GSH and SOD at 3 days post injury.…”

Section: Discussionsupporting

confidence: 94%

The Effects of Icariin on Enhancing Motor Recovery Through Attenuating Pro-inflammatory Factors and Oxidative Stress via Mitochondrial Apoptotic Pathway in the Mice Model of Spinal Cord Injury

Zhang

et al. 2018

Front. Physiol.

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Spinal cord injury (SCI) is a severe medical problem leading to crucial life change. Icariin (ICA) is a natural flavonoid compound extracted from the Chinese herb Epimedium brevicornum which has neuroprotective effects. But little is known about the relationship between ICA and SCI. We hypothesized ICA may enhance motor recovery through attenuating inflammation, oxidative stress and mitochondrial dysfunction. Mice were randomly assigned to sham, SCI, ICA 20 μmol/kg (low dose) and ICA 50 μmol/kg (high dose) groups. And Behavioral, biochemical, molecular biological, immunofluorescent and histological assays were performed. First, ICA enhanced motor recovery greatly at 14, 28, and 42 days and protected spinal cord tissues especially in the high dose group. Meanwhile, ICA decreased the production of interleukin-1 beta, tumor necrosis factor-alpha and inducible nitric oxide synthase at 24 h and 3 days after SCI. The level of mitochondrial reduced glutathione, superoxide dismutase, adenosine triphosphate (ATP), Na+-K+-ATPase, mitochondrial membrane potential, state III respiration rate and the respiratory control ratio were also significantly increased, while malondialdehyde level and Ca2+ concentration were decreased by ICA. Furthermore, ICA decreased the expression of mitochondrial apoptotic proteins at 3 days after SCI. More importantly, transferase UTP nick end labeling (TUNEL) and Nissl staining implied that ICA at a high dose inhibited the neuronal apoptosis after SCI. Our research indicated that early and continuous treatment of ICA at a high dose significantly enhanced motor recovery after SCI through inhibiting pro-inflammatory factors, oxidative stress and neuronal apoptosis via mitochondrial apoptotic pathway.

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Section: Discussionsupporting

confidence: 94%

The Effects of Icariin on Enhancing Motor Recovery Through Attenuating Pro-inflammatory Factors and Oxidative Stress via Mitochondrial Apoptotic Pathway in the Mice Model of Spinal Cord Injury

Zhang

et al. 2018

Front. Physiol.

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“…In contrast, mitochondrial fission resulting from mitochondrial dysfunction further inhibits microtubule stabilization and axonal regeneration and is associated with apoptosis (Csordás et al, 2018 ). The dysfunction of mitochondrial fission and fusion caused by SCI is associated with the upregulation of Drp1, which reduces mitochondrial membrane potential, releases cytochrome C and caspase3, and induces neuronal apoptosis (Jia et al, 2016 ).…”

Section: Injurymentioning

confidence: 99%

“…In an SCI model, Loureirin B significantly increased both bcl-2 and Mfn1 and doubled the size of the mitochondria, which promoted fusion and facilitated axon regeneration (Wang et al, 2019a ). Considering the adverse effects of Drp1 upregulation after SCI injury, mitochondrial division inhibitor-1, an inhibitor of Drp1, promotes animal recovery and reduces apoptosis (Jia et al, 2016 ).…”

Section: Injurymentioning

confidence: 99%

Mitochondrial Behavior in Axon Degeneration and Regeneration

Wang

Huang

Shang

et al. 2021

Front. Aging Neurosci.

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Mitochondria are organelles responsible for bioenergetic metabolism, calcium homeostasis, and signal transmission essential for neurons due to their high energy consumption. Accumulating evidence has demonstrated that mitochondria play a key role in axon degeneration and regeneration under physiological and pathological conditions. Mitochondrial dysfunction occurs at an early stage of axon degeneration and involves oxidative stress, energy deficiency, imbalance of mitochondrial dynamics, defects in mitochondrial transport, and mitophagy dysregulation. The restoration of these defective mitochondria by enhancing mitochondrial transport, clearance of reactive oxidative species (ROS), and improving bioenergetic can greatly contribute to axon regeneration. In this paper, we focus on the biological behavior of axonal mitochondria in aging, injury (e.g., traumatic brain and spinal cord injury), and neurodegenerative diseases (Alzheimer's disease, AD; Parkinson's disease, PD; Amyotrophic lateral sclerosis, ALS) and consider the role of mitochondria in axon regeneration. We also compare the behavior of mitochondria in different diseases and outline novel therapeutic strategies for addressing abnormal mitochondrial biological behavior to promote axonal regeneration in neurological diseases and injuries.

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“…Mitochondria function and morphology changes, including irregular shape, enlarged size, disordered cristae, fusion and fission, reduced membrane potential, and expression changes of related proteins occur in the acute phase after SCI. Furthermore, these morphological and functional changes regulate underlying secondary injury processes, such as necrosis, apoptosis, and autophagy [ 14 ]. Mitochondrial dysfunction influences secondary injury development and neuronal cell death [ 13 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

CD157 in bone marrow mesenchymal stem cells mediates mitochondrial production and transfer to improve neuronal apoptosis and functional recovery after spinal cord injury

Cai

et al. 2021

Stem Cell Res Ther

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Background Recent studies demonstrated that autologous mitochondria derived from bone marrow mesenchymal stem cells (BMSCs) might be valuable in the treatment of spinal cord injury (SCI). However, the mechanisms of mitochondrial transfer from BMSCs to injured neurons are not fully understood. Methods We modified BMSCs by CD157, a cell surface molecule as a potential regulator mitochondria transfer, then transplanted to SCI rats and co-cultured with OGD injured VSC4.1 motor neuron. We detected extracellular mitochondrial particles derived from BMSCs by transmission electron microscope and measured the CD157/cyclic ADP-ribose signaling pathway-related protein expression by immunohistochemistry and Western blotting assay. The CD157 ADPR-cyclase activity and Fluo-4 AM was used to detect the Ca2+ signal. All data were expressed as mean ± SEM. Statistical analysis was analyzed by GraphPad Prism 6 software. Unpaired t-test was used for the analysis of two groups. Multiple comparisons were evaluated by one-way ANOVA or two-way ANOVA. Results CD157 on BMSCs was upregulated when co-cultured with injured VSC4.1 motor neurons. Upregulation of CD157 on BMSCs could raise the transfer extracellular mitochondria particles to VSC4.1 motor neurons, gradually regenerate the axon of VSC4.1 motor neuron and reduce the cell apoptosis. Transplantation of CD157-modified BMSCs at the injured sites could significantly improve the functional recovery, axon regeneration, and neuron apoptosis in SCI rats. The level of Ca2+ in CD157-modified BMSCs dramatically increased when objected to high concentration cADPR, ATP content, and MMP of BMSCs also increased. Conclusion The present results suggested that CD157 can regulate the production and transfer of BMSC-derived extracellular mitochondrial particles, enriching the mechanism of the extracellular mitochondrial transfer in BMSCs transplantation and providing a novel strategy to improve the stem cell treatment on SCI.

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Time representation of mitochondrial morphology and function after acute spinal cord injury

Cited by 31 publications

References 40 publications

The Effects of Icariin on Enhancing Motor Recovery Through Attenuating Pro-inflammatory Factors and Oxidative Stress via Mitochondrial Apoptotic Pathway in the Mice Model of Spinal Cord Injury

The Effects of Icariin on Enhancing Motor Recovery Through Attenuating Pro-inflammatory Factors and Oxidative Stress via Mitochondrial Apoptotic Pathway in the Mice Model of Spinal Cord Injury

Mitochondrial Behavior in Axon Degeneration and Regeneration

CD157 in bone marrow mesenchymal stem cells mediates mitochondrial production and transfer to improve neuronal apoptosis and functional recovery after spinal cord injury

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