Brain self-protection: The role of endogenous neural progenitor cells in adult brain after cerebral cortical ischemia

Li, Bin; Piao, Chun Shu; Liu, Xiaoyun; Guo, Wen Ping; Xue, Yue Qiang; Duan, Wei; Gonzalez-Toledo, Maria E.; Zhao, Li

doi:10.1016/j.brainres.2010.02.030

Cited by 48 publications

(48 citation statements)

References 37 publications

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“…Given the safety and ethical issues of exogenous cell transplantation, activation of endogenous NSCs as an alternative therapy is an ideal repair method for CNS injury. The endogenous progenitor cells might work as a potential self-protection mechanism in brain ischemia [9]. Studies have demonstrated that in ischemia, trauma, and nerve injury, a large number of endogenous NSCs are activated, their proliferation and differentiation levels are significantly increased, and they participate in the injured body's natural recovery process [10].…”

Section: Discussionmentioning

confidence: 99%

Curcumin increased the differentiation rate of neurons in neural stem cells via wnt signaling in vitro study

Chen

Wang

Xiang

et al. 2014

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

Curcumin increased the differentiation rate of neurons in neural stem cells via wnt signaling in vitro study

Chen

Wang

Xiang

et al. 2014

Journal of Surgical Research

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“…It has been shown that focal cerebral ischemia causes increase of NSC/NPC proliferation in both the SVZ and SGZ during the 4 days to 2 weeks after ischemia (Arvidsson et al, 2002; Jin et al, 2001; Li et al, 2010). By contrast to the ordinary migratory pathway through the RMS, the SVZ-derived NSCs/NPCs and neuroblast can directly migrate to the peri-infarct cortex (Leker et al, 2007) and peri-infarct striatum (Arvidsson et al, 2002) along the corpus callosum (Leker et al, 2007; Li et al, 2010), astrocyte processes (Yamashita et al, 2006), and blood vessels (Thored et al, 2007; Yamashita et al, 2006).…”

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

confidence: 99%

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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“…32 Although there is an upregulation of BDNF expression after neuronal damage in adult rodents, the amount of BDNF is not sufficient to promote recovery. 33 Hence, exogenous supplementation with BDNF could be beneficial in that regard. In our injury model, BDNF mRNA levels in the retina significantly decreased 6 to 24 hours after HI injury.…”

Section: / Chx10mentioning

confidence: 99%

Systemic 7,8-Dihydroxyflavone Treatment Protects Immature Retinas Against Hypoxic-Ischemic Injury via Müller Glia Regeneration and MAPK/ERK Activation

Huang

Tsai

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Perinatal hypoxic-ischemic (HI) injury causes significant damages in the immature retina. The brain-derived neurotrophic factor is well known for its neuroprotective role but has limited clinical applications. A selective agonist of tyrosine kinase receptor B, 7,8-dihydroxyflavone (DHF), is a powerful therapeutic tool, when administered systemically. However, it remains unclear whether DHF treatment can protect the immature retinas against HI injury.METHODS. Postnatal (P) day 7 rat pups were intraperitoneally injected with DHF or vehicle 2 hours before and 18 hours after being subjected to HI injury. The outcomes were assessed at various timepoints after injury by electroretinography and histologic examinations. Neurogenesis was assessed by double-labeling of retinal sections with 5-bromo-2 0 -deoxyuridine and different neuronal markers.RESULTS. At P8, 24-hours postinjury, brain-derived neurotrophic factor mRNA levels in the retina decreased significantly. DHF treatment partially protected immature retinas at both histologic and functional levels between P14 and P30 but did not prevent apoptosis, inflammation, or damage of the blood-retinal barrier (BRB) at P8. On the other hand, DHF treatment promoted the survival of proliferating inner retinal cells, including Müller glia, and enhanced their transdifferentiation to bipolar cells at P17. Moreover, DHF treatment rescued the levels of extracellular signal-regulated kinase (ERK) phosphorylation, which were significantly decreased after injury. The neuroprotective effects of DHF were markedly eliminated by inhibition of ERK phosphorylation.CONCLUSIONS. Early systemic DHF treatment has neuroprotective effects against HI injury in immature retinas, possibly via promoting neurogenesis through the tyrosine kinase receptor B/ERK signaling pathway.

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Brain self-protection: The role of endogenous neural progenitor cells in adult brain after cerebral cortical ischemia

Cited by 48 publications

References 37 publications

Curcumin increased the differentiation rate of neurons in neural stem cells via wnt signaling in vitro study

Curcumin increased the differentiation rate of neurons in neural stem cells via wnt signaling in vitro study

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

Systemic 7,8-Dihydroxyflavone Treatment Protects Immature Retinas Against Hypoxic-Ischemic Injury via Müller Glia Regeneration and MAPK/ERK Activation

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