Electroacupuncture stimulates the proliferation and differentiation of endogenous neural stem cells in a rat model of ischemic stroke

Tan, Feng; Wang, Jian; Liu, Jing Xian; Wang, Chen; Li, Miaodan; Gu, Yong

doi:10.3892/etm.2018.6848

Cited by 10 publications

(7 citation statements)

References 39 publications

(49 reference statements)

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“…EA directly upregulated the gene expression of plasticity-related gene 5 (PRG5), which is a critical neurogenesis factor, and also upregulated the protein expression of postsynaptic density 95 (PSD95) and synaptophysin (SYP). Moreover, EA downregulated the expression of neurogenesis inhibitory molecules, including NogoA, lysophosphatidic acid, and RhoA, to improve the proliferation and differentiation of endogenous neural stem cells and synaptic plasticity in stroke rats ( Tan et al, 2018 ; Yang et al, 2022 ). Deng et al (2021) have reported that EA promoted differentiation of transplanted MSCs into neuron-like cells and expressions of BDNF and NGF proteins displaying therapeutic efficacy in ICH rats.…”

Section: Mechanisms Of Mesenchymal Stem Cells In Intracerebral Hemorr...mentioning

confidence: 99%

Mesenchymal Stem Cell Application and Its Therapeutic Mechanisms in Intracerebral Hemorrhage

Yang

Fan

Mazhar

et al. 2022

Front. Cell. Neurosci.

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Intracerebral hemorrhage (ICH), a common lethal subtype of stroke accounting for nearly 10–15% of the total stroke disease and affecting two million people worldwide, has a high mortality and disability rate and, thus, a major socioeconomic burden. However, there is no effective treatment available currently. The role of mesenchymal stem cells (MSCs) in regenerative medicine is well known owing to the simplicity of acquisition from various sources, low immunogenicity, adaptation to the autogenic and allogeneic systems, immunomodulation, self-recovery by secreting extracellular vesicles (EVs), regenerative repair, and antioxidative stress. MSC therapy provides an increasingly attractive therapeutic approach for ICH. Recently, the functions of MSCs such as neuroprotection, anti-inflammation, and improvement in synaptic plasticity have been widely researched in human and rodent models of ICH. MSC transplantation has been proven to improve ICH-induced injury, including the damage of nerve cells and oligodendrocytes, the activation of microglia and astrocytes, and the destruction of blood vessels. The improvement and recovery of neurological functions in rodent ICH models were demonstrated via the mechanisms such as neurogenesis, angiogenesis, anti-inflammation, anti-apoptosis, and synaptic plasticity. Here, we discuss the pathological mechanisms following ICH and the therapeutic mechanisms of MSC-based therapy to unravel new cues for future therapeutic strategies. Furthermore, some potential strategies for enhancing the therapeutic function of MSC transplantation have also been suggested.

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Section: Mechanisms Of Mesenchymal Stem Cells In Intracerebral Hemorr...mentioning

confidence: 99%

Mesenchymal Stem Cell Application and Its Therapeutic Mechanisms in Intracerebral Hemorrhage

Yang

Fan

Mazhar

et al. 2022

Front. Cell. Neurosci.

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“…Thomas Broggini suggested that plppr5 , as an upstream molecule of ROCK, can overcome LPA and Nogo-A-induced neurite contraction caused by RhoA-ROCK-PIP5K kinase pathway activation ( 16 ). Recently, Tan et al found that electroacupuncture stimulation may be involved in the neuroprotective effect of cerebral ischemia-reperfusion rats mediated through plppr5/NogoA-LPA/RhoA signaling ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

Effects of Melatonin on Neurobehavior and Cognition in a Cerebral Palsy Model of plppr5−/− Mice

Sun

Jin

et al. 2021

Front. Endocrinol.

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Cerebral palsy (CP), a group of clinical syndromes caused by non-progressive brain damage in the developing fetus or infant, is one of the most common causes of lifelong physical disability in children in most countries. At present, many researchers believe that perinatal cerebral hypoxic ischemic injury or inflammatory injury are the main causes of cerebral palsy. Previous studies including our works confirmed that melatonin has a protective effect against convulsive brain damage during development and that it affects the expression of various molecules involved in processes such as metabolism, plasticity and signaling in the brain. Integral membrane protein plppr5 is a new member of the plasticity-related protein family, which is specifically expressed in brain and spinal cord, and induces filopodia formation as well as neurite growth. It is highly expressed in the brain, especially in areas of high plasticity, such as the hippocampus. The signals are slightly lower in the cortex, the cerebellum, and in striatum. Noteworthy, during development plppr5 mRNA is expressed in the spinal cord, i.e., in neuron rich regions such as in medial motor nuclei, suggesting that plppr5 plays an important role in the regulation of neurons. However, the existing literature only states that plppr5 is involved in the occurrence and stability of dendritic spines, and research on its possible involvement in neonatal ischemic hypoxic encephalopathy has not been previously reported. We used plppr5 knockout (plppr5−/−) mice and their wild-type littermates to establish a model of hypoxicischemic brain injury (HI) to further explore the effects of melatonin on brain injury and the role of plppr5 in this treatment in an HI model, which mainly focuses on cognition, exercise, learning, and memory. All the tests were performed at 3–4 weeks after HI. As for melatonin treatment, which was performed 5 min after HI injury and followed by every 24h. In these experiments, we found that there was a significant interaction between genotype and treatment in novel object recognition tests, surface righting reflex tests and forelimb suspension reflex tests, which represent learning and memory, motor function and coordination, and the forelimb grip of the mice, respectively. However, a significant main effect of genotype and treatment on performance in all behavioral tests were observed. Specifically, wild-type mice with HI injury performed better than plppr5−/− mice, regardless of treatment with melatonin or vehicle. Moreover, treatment with melatonin could improve behavior in the tests for wild-type mice with HI injury, but not for plppr5−/− mice. This study showed that plppr5 knockout aggravated HI damage and partially weakened the neuroprotection of melatonin in some aspects (such as novel object recognition test and partial nerve reflexes), which deserves further study.

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“…The Nissl bodies (blue) staining in neural cells were clearly visible and distinct. Cells with Nissl staining in the cytoplasm and prominent nucleoli were identified as surviving neurones, whilst cells with shrunken shape, cavitation around the nucleus or loss of Nissl substance were considered damaged ( 43 ). Only whole neurones with visible nuclei were counted.…”

Section: Methodsmentioning

confidence: 99%

Repetitive transcranial magnetic stimulation increases neurological function and endogenous neural stem cell migration via the SDF‑1α/CXCR4 axis after cerebral infarction in rats

et al. 2021

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Neural stem cell (NSC) migration is closely associated with brain development and is reportedly involved during recovery from ischaemic stroke. Chemokine signalling mediated by stromal cell-derived factor 1α (SDF-1α) and its receptor CXC chemokine receptor 4 (CXCR4) has been previously documented to guide the migration of NSCs. Although repetitive transcranial magnetic stimulation (rTMS) can increase neurological function in a rat stroke model, its effects on the migration of NSCs and associated underlying mechanism remain unclear. Therefore, the present study investigated the effects of rTMS on ischaemic stroke following middle cerebral artery occlusion (MCAO). All rats underwent rTMS treatment 24 h after MCAO. Neurological function, using modified Neurological Severity Scores and grip strength test and NSC migration, which were measured using immunofluorescence staining, were analysed at 7 and 14 days after MCAO, before the protein expression levels of the SDF-1α/CXCR4 axis was evaluated using western blot analysis. AMD3100, a CXCR4 inhibitor, was used to assess the effects of SDF-1α/CXCR4 signalling. In addition, neuronal survival was investigated using Nissl staining at 14 days after MCAO. It was revealed that rTMS increased the neurological recovery of rats with MCAO, facilitated the migration of NSC, augmented the expression levels of the SDF-1α/CXCR4 axis and decreased neuronal loss. Furthermore, the rTMS-induced positive responses were significantly abolished by AMD3100. Overall, these results indicated that rTMS conferred therapeutic neuroprotective properties, which can restore neurological function after ischaemic stroke, in a manner that may be associated with the activation of the SDF-1α/CXCR4 axis.

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Electroacupuncture stimulates the proliferation and differentiation of endogenous neural stem cells in a rat model of ischemic stroke

Cited by 10 publications

References 39 publications

Mesenchymal Stem Cell Application and Its Therapeutic Mechanisms in Intracerebral Hemorrhage

Mesenchymal Stem Cell Application and Its Therapeutic Mechanisms in Intracerebral Hemorrhage

Effects of Melatonin on Neurobehavior and Cognition in a Cerebral Palsy Model of plppr5−/− Mice

Repetitive transcranial magnetic stimulation increases neurological function and endogenous neural stem cell migration via the SDF‑1α/CXCR4 axis after cerebral infarction in rats

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