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Endogenous bioelectric fields: a putative regulator of wound repair and regeneration in the central nervous system 被引量:1
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作者 Matthew L.Baer Raymond J.Colello 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第6期861-864,共4页
Studies on a variety of highly regenerative tissues, including the central nervous system(CNS) in non-mammalian vertebrates, have consistently demonstrated that tissue damage induces the formation of an ionic curren... Studies on a variety of highly regenerative tissues, including the central nervous system(CNS) in non-mammalian vertebrates, have consistently demonstrated that tissue damage induces the formation of an ionic current at the site of injury. These injury currents generate electric fields(EF) that are 100-fold increased in intensity over that measured for uninjured tissue. In vitro and in vivo experiments have convincingly demonstrated that these electric fields(by their orientation, intensity and duration) can drive the migration, proliferation and differentiation of a host of cell types. These cellular behaviors are all necessary to facilitate regeneration as blocking these EFs at the site of injury inhibits tissue repair while enhancing their intensity promotes repair. Consequently, injury-induced currents, and the EFs they produce, represent a potent and crucial signal to drive tissue regeneration and repair. In this review, we will discuss how injury currents are generated, how cells detect these currents and what cellular responses they can induce. Additionally, we will describe the growing evidence suggesting that EFs play a key role in regulating the cellular response to injury and may be a therapeutic target for inducing regeneration in the mammalian CNS. 展开更多
关键词 repair regeneration currents inducing consistently regulating migration potent wound facilitate
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Acetylation as a mechanism that regulates axonal regeneration
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作者 Shen Lin George M.Smith 《Neural Regeneration Research》 SCIE CAS CSCD 2015年第7期1034-1036,共3页
The capacity for adult axons to regenerate after injury is diminished compared with developing axons.In the case of central nervous system(CNS)axons,injury causes a total failure to regenerate.This failure is due to... The capacity for adult axons to regenerate after injury is diminished compared with developing axons.In the case of central nervous system(CNS)axons,injury causes a total failure to regenerate.This failure is due to both the intrinsic developmental decrease in growth capacity and the extrinsic inhibitory environment formed because of the injury. 展开更多
关键词 GENE HDAC Acetylation as a mechanism that regulates axonal regeneration
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Specific effects of c-Jun NH2-terminal kinaseinteracting protein 1 in neuronal axons 被引量:1
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作者 Shu Tang Qiang Wen +1 位作者 Xiao-jian Zhang Quan-cheng Kan 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第1期114-118,共5页
c-Jun NH2-terminal kinase(JNK)-interacting protein 3 plays an important role in brain-derived neurotrophic factor/tropomyosin-related kinase B(Trk B) anterograde axonal transport. It remains unclear whether JNK-in... c-Jun NH2-terminal kinase(JNK)-interacting protein 3 plays an important role in brain-derived neurotrophic factor/tropomyosin-related kinase B(Trk B) anterograde axonal transport. It remains unclear whether JNK-interacting protein 1 mediates similar effects, or whether JNK-interacting protein 1 affects the regulation of Trk B anterograde axonal transport. In this study, we isolated rat embryonic hippocampus and cultured hippocampal neurons in vitro. Coimmunoprecipitation results demonstrated that JNK-interacting protein 1 formed Trk B complexes in vitro and in vivo. Immunocytochemistry results showed that when JNK-interacting protein 1 was highly expressed, the distribution of Trk B gradually increased in axon terminals. However, the distribution of Trk B reduced in axon terminals after knocking out JNK-interacting protein 1. In addition, there were differences in distribution of Trk B after JNK-interacting protein 1 was knocked out compared with not. However, knockout of JNK-interacting protein 1 did not affect the distribution of Trk B in dendrites. These findings confirm that JNK-interacting protein 1 can interact with Trk B in neuronal cells, and can regulate the transport of Trk B in axons, but not in dendrites. 展开更多
关键词 nerve regeneration c-Jun NH2-terminal kinase-interacting protein neurons brain-derived neurotrophic factor tropomyosin-related kinase B axons hippocampus dendrites regulation neural regeneration
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Correlation between receptor-interacting protein 140 expression and directed differentiation of human embryonic stem cells into neural stem cells 被引量:3
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作者 Zhu-ran Zhao Wei-dong Yu +7 位作者 Cheng Shi Rong Liang Xi Chen Xiao Feng Xue Zhang Qing Mu Huan Shen Jing-zhu Guo 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第1期118-124,共7页
Overexpression of receptor-interacting protein 140(RIP140) promotes neuronal differentiation of N2 a cells via extracellular regulated kinase 1/2(ERK1/2) signaling.However,involvement of RIP140 in human neural dif... Overexpression of receptor-interacting protein 140(RIP140) promotes neuronal differentiation of N2 a cells via extracellular regulated kinase 1/2(ERK1/2) signaling.However,involvement of RIP140 in human neural differentiation remains unclear.We found both RIP140 and ERK1/2 expression increased during neural differentiation of H1 human embryonic stem cells.Moreover,RIP140 negatively correlated with stem cell markers Oct4 and Sox2 during early stages of neural differentiation,and positively correlated with the neural stem cell marker Nestin during later stages.Thus,ERK1/2 signaling may provide the molecular mechanism by which RIP140 takes part in neural differentiation to eventually affect the number of neurons produced. 展开更多
关键词 nerve regeneration receptor-interacting protein 140 neural stem cells human embryonic stem cells directed differentiation Oct4 Sox2 Nestin extracellular regulated kinase 1/2 signaling pathway neural regeneration
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Microenvironment of Liver Regeneration in Liver Cancer 被引量:20
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作者 LI Han-min YE Zhi-hua 《Chinese Journal of Integrative Medicine》 SCIE CAS CSCD 2017年第7期555-560,共6页
The occurrence and development of liver cancer are essentially the most serious outcomes of uncontrolled liver regeneration. The progression of liver cancer is inevitably related to the abnormal microenvironment of li... The occurrence and development of liver cancer are essentially the most serious outcomes of uncontrolled liver regeneration. The progression of liver cancer is inevitably related to the abnormal microenvironment of liver regeneration. The deterioration observed in the microenvironment of liver regeneration is a necessary condition for the occurrence, development and metastasis of cancer. Therefore, the use of a technique to prevent and treat liver cancer via changes in the microenvironment of liver regeneration is a novel strategy. This strategy would be an effective way to delay, prevent or even reverse cancer occurrence, development and metastasis through an improvement in the liver regeneration microenvironment along with the integrated regulation of multiple components, targets, levels, channels and time sequences. In addition, the treatment of "tonifying Shen(Kidney) to regulate liver regeneration and repair by affecting stem cells and their microenvironment" can regulate "the dynamic imbalance between the normal liver regeneration and the abnormal liver regeneration"; this would improve the microenvironment of liver regeneration, which is also a mechanism by which liver cancer may be prevented or treated. 展开更多
关键词 liver regeneration microenvironment liver cancer tonifying Shen(Kidney) to regulate liver regeneration and repair by affecting stem cells and their microenvironment
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