NF-κB is involved in brain repair by stem cell factor and granulocyte-colony stimulating factor in chronic stroke

Cui, Lili; Duchamp, Nicolas S.; Boston, Dakota J.; Ren, Xuefang; Zhang, Xiangjian; Hu, Heng; Zhao, Li-Ru

doi:10.1016/j.expneurol.2014.08.026

Cited by 50 publications

(50 citation statements)

References 35 publications

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“…The SCF + G-CSF-induced restorative changes in the peri-infarct-cavity cortex include increases in dendritic spine size, PSD-95 accumulation (PSD-95: a key postsynaptic protein involved in synaptic function), presynaptic vesicle protein, dendritic branching, axonal sprouting, and blood vessel density. The SCF + G-CSF-enhanced neurovascular network remodeling has been conformed in young and aged animals, and when treatment is initiated during 3 to 6 months after experimental stroke (Cui et al, 2015; Cui et al, 2013; Cui et al, 2016; Piao et al, 2012a; Piao et al, 2009; Zhao et al, 2007a; Zhao et al, 2013). It has been shown that bone marrow-derived endothelial cells and bone marrow-derived neurons are involved in SCF + G-CSF-enhanced angiogenesis and neurogenesis in the brain of chronic stroke (Piao et al, 2009).…”

Section: Putative Therapies For Enhancing Brain Self-repair and Strokmentioning

confidence: 98%

“…Modification in synaptic circuits or synaptic connections may be involved in functional reorganization and neural network remodeling in the brain after stroke (Brown et al, 2007; Brown et al, 2008; Cui et al, 2015; Cui et al, 2016). …”

Section: The Intrinsic Capability Of Brain Self-repair In Stroke Recomentioning

confidence: 99%

“…SCF and G-CSF intervention in chronic stroke for enhancing functional improvement has been tested and validated to be safe and effective when administered 3 to 6 months after cerebral cortical ischemia in both young and aged spontaneously hypertensive rats (SHRs), C57BL mice, or transgenic mice with C57BL genetic background (Cui et al, 2015; Cui et al, 2013; Cui et al, 2016; Liu et al, 2016; Piao et al, 2012a; Piao et al, 2009; Zhao et al, 2007a). SCF + G-CSF combination shows a stable and long-term effect in the enhancement of brain repair and motor function recovery when compared with SCF and G-CSF alone (Zhao et al, 2007a).…”

Section: Putative Therapies For Enhancing Brain Self-repair and Strokmentioning

confidence: 99%

“…3). A study using an anterograde axonal tracer reveals that SCF + G-CSF treatment in the chronic phase promotes axonal sprouting of the contralesional cortical neurons projecting into the peri-infarct-cavity cortex (Cui et al, 2015). Interestingly, SCF + G-CSF treatment also shows an “over-increase” of dendritic spine head size and PSD-95 accumulation in the peri-infarct-cavity cortex as compared to intact or unaffected brains, suggesting that SCF + G-CSF-enhanced robust synaptic activity occurs in the surviving neurons next to the infarct cavity for taking over the function of the lost neurons (Cui et al, 2015; Cui et al, 2016).…”

Section: Putative Therapies For Enhancing Brain Self-repair and Strokmentioning

confidence: 99%

“…However, recent clinical and preclinical studies have challenged this old notion. Emerging evidence has shown that the advanced physical rehabilitation approach and pharmaceutical intervention can enhance functional improvement when administered in the chronic phase (Cui et al, 2015; Cui et al, 2016; Lee et al, 2015; Park and Park, 2016; Piao et al, 2012a; Zhao et al, 2007a; Zittel et al, 2007). …”

Section: Introductive Remarks: the Importance Of Enhancing Stroke Recmentioning

confidence: 99%

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Enhancing endogenous capacity to repair a stroke-damaged brain: An evolving field for stroke research

Zhao

Willing

2018

Progress in Neurobiology

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102

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Stroke represents a severe medical condition that causes stroke survivors to suffer from long-term and even lifelong disability. Over the past several decades, a vast majority of stroke research targets neuroprotection in the acute phase, while little work has been done to enhance stroke recovery at the later stage. Through reviewing current understanding of brain plasticity, stroke pathology, and emerging preclinical and clinical restorative approaches, this review aims to provide new insights to advance the research field for stroke recovery. Lifelong brain plasticity offers the long-lasting possibility to repair a stroke-damaged brain. Stroke impairs the structural and functional integrity of entire brain networks; the restorative approaches containing multi-components have great potential to maximize stroke recovery by rebuilding and normalizing the stroke-disrupted entire brain networks and brain functioning. The restorative window for stroke recovery is much longer than previously thought. The optimal time for brain repair appears to be at later stage of stroke rather than the earlier stage. It is expected that these new insights will advance our understanding of stroke recovery and assist in developing the next generation of restorative approaches for enhancing brain repair after stroke.

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Section: Putative Therapies For Enhancing Brain Self-repair and Strokmentioning

confidence: 98%

Section: The Intrinsic Capability Of Brain Self-repair In Stroke Recomentioning

confidence: 99%

Section: Putative Therapies For Enhancing Brain Self-repair and Strokmentioning

confidence: 99%

Section: Putative Therapies For Enhancing Brain Self-repair and Strokmentioning

confidence: 99%

Section: Introductive Remarks: the Importance Of Enhancing Stroke Recmentioning

confidence: 99%

See 3 more Smart Citations

Enhancing endogenous capacity to repair a stroke-damaged brain: An evolving field for stroke research

Zhao

Willing

2018

Progress in Neurobiology

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102

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Role of liraglutide in brain repair promotion through Sirt1‐mediated mitochondrial improvement in stroke

Wang

Zhao

et al. 2019

Journal Cellular Physiology

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Brain repair, especially axonal sprouting, is critical to restore motor function in disabled stroke patients. Liraglutide (LG) is a new kind of long-acting analogue of glucagon-like peptide-1 (GLP-1) and has potential protective effects in stroke. The mitochondria participate in brain repair after cerebral injury. However, the mechanism of the effect of LG on brain repair and its potential influence on mitochondria in stroke remains obscure. Here, in focal cerebral cortical ischemic mice model, LG improved the motor functional recovery and promoted axonal sprouting by restoring the activities of isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, and succinate dehydrogenase. Moreover, LG remarkably increased the cell survival rate and revived the NeuN and GAP-43 levels in cortical neurons under hydrogen peroxide (H 2 O 2 ) exposure. It was also observed that LG reduced the generation of reactive oxygen species, stabilized the mitochondrial membrane potential, enhanced the levels of adenosine triphosphate, enhanced activities of mitochondrial complex-I, and decreased protein expression levels of fission-1 in H 2 O 2 -injured cortical neurons.Additionally, LG suppressed the expressions of sirtuin 1 (Sirt1) in cortical neurons exposed to H 2 O 2 . Furthermore, knockdown of Sirt1 by short interfering RNA facilitated the LG-mediated mitochondrial protection in cortical neurons under H 2 O 2 .Collectively, this data from the present study illustrated that LG exerted a promoting influence on brain repair, after cerebral ischemic injury, through Sirt1-mediated mitochondrial improvement.

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MTEP impedes the neuronal polarization and the activity of the Akt–NF‐κB pathway in rat hippocampal neurons

Zhang

Zhang³

et al. 2016

J of Neuroscience Research

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Metabotropic glutamate receptor 5 (mGluR5) is extensively involved in neural survival, differentiation, dendritic morphology, synaptic plasticity, and neural circuit formation. However, little is known about its role in neuronal polarization and axon outgrowth. In this study, we applied the selective agonist (RS)-2-chloro-5-hydroxyphenylglycine sodium salt and antagonist 3-[(2-methyl-4-thaizolyl) ethynyl] pyridine (MTEP) of mGluR5 to the cultured hippocampal neurons to observe the neuronal polarization and axon outgrowth, and further explored the possible intracellular signal transduction pathway. The results demonstrated that MTEP administration significantly attenuates the proportion of polarized neurons and the length of the axon, indicated by SMI312 (an axon marker) and Tuj-1 (a marker of all the neurites) double-labeling immunofluorescence. Western blot analysis showed that MTEP administration also inhibited the activation of AKT and nuclear translocation of nuclear factor-κB (NF-κB) p65, and decreased the phosphorylation of p65 as well. Furthermore, Akt inhibitor LY294002 treatment resulted in neuronal polarization delay and axon outgrowth retardation, while suppressing the phosphorylation and nuclear translocation of p65. We concluded that mGluR5 could regulate neuronal polarity and axon outgrowth during the morphological differentiation of rat developing neurons, and the intracellular signaling pathway of Akt-NF-κB might be involved in the action of mGluR5. © 2016 Wiley Periodicals, Inc.

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NF-κB is involved in brain repair by stem cell factor and granulocyte-colony stimulating factor in chronic stroke

Cited by 50 publications

References 35 publications

Enhancing endogenous capacity to repair a stroke-damaged brain: An evolving field for stroke research

Enhancing endogenous capacity to repair a stroke-damaged brain: An evolving field for stroke research

Role of liraglutide in brain repair promotion through Sirt1‐mediated mitochondrial improvement in stroke

MTEP impedes the neuronal polarization and the activity of the Akt–NF‐κB pathway in rat hippocampal neurons

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