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Selective deletion of zinc transporter 3 in amacrine cells promotes retinal ganglion cell survival and optic nerve regeneration after injury 被引量:2
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作者 Zhe Liu Jingfei Xue +10 位作者 Canying Liu Jiahui Tang Siting Wu jicheng lin Jiaxu Han Qi Zhang Caiqing Wu Haishun Huang ling Zhao Yehong Zhuo Yiqing Li 《Neural Regeneration Research》 SCIE CAS CSCD 2023年第12期2773-2780,共8页
Vision depends on accurate signal conduction from the retina to the brain through the optic nerve,an important part of the central nervous system that consists of bundles of axons originating from retinal ganglion cel... Vision depends on accurate signal conduction from the retina to the brain through the optic nerve,an important part of the central nervous system that consists of bundles of axons originating from retinal ganglion cells.The mammalian optic nerve,an important part of the central nervous system,cannot regenerate once it is injured,leading to permanent vision loss.To date,there is no clinical treatment that can regenerate the optic nerve and restore vision.Our previous study found that the mobile zinc(Zn^(2+))level increased rapidly after optic nerve injury in the retina,specifically in the vesicles of the inner plexiform layer.Furthermore,chelating Zn^(2+)significantly promoted axonal regeneration with a long-term effect.In this study,we conditionally knocked out zinc transporter 3(ZnT3)in amacrine cells or retinal ganglion cells to construct two transgenic mouse lines(VGAT^(Cre)ZnT3^(fl/fl)and VGLUT2^(Cre)ZnT3^(fl/fl),respectively).We obtained direct evidence that the rapidly increased mobile Zn^(2+)in response to injury was from amacrine cells.We also found that selective deletion of ZnT3 in amacrine cells promoted retinal ganglion cell survival and axonal regeneration after optic nerve crush injury,improved retinal ganglion cell function,and promoted vision recovery.Sequencing analysis of reginal ganglion cells revealed that inhibiting the release of presynaptic Zn^(2+)affected the transcription of key genes related to the survival of retinal ganglion cells in postsynaptic neurons,regulated the synaptic connection between amacrine cells and retinal ganglion cells,and affected the fate of retinal ganglion cells.These results suggest that amacrine cells release Zn^(2+)to trigger transcriptomic changes related to neuronal growth and survival in reginal ganglion cells,thereby influencing the synaptic plasticity of retinal networks.These results make the theory of zinc-dependent retinal ganglion cell death more accurate and complete and provide new insights into the complex interactions between retinal cell networks. 展开更多
关键词 axonal regeneration conditional knockout NEUROTRANSMITTER optic nerve injury presynaptic neuron retinal network synaptic connection synaptic vesicles visual acuity zinc transporter 3
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Teaching Research and Reform of Higher Vocational Medical Education in Guizhou Province of China
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作者 Wan Ding jicheng lin +3 位作者 Jianhui Yang Xianming Cao Fang Cao Shaomei Lu 《Journal of Advances in Medicine Science》 2019年第2期1-7,共7页
With the development of Guizhou’s economy and society, higher vocational medical education in Guizhou has developed rapidly, making it its mission to cultivate practical and skilled talents oriented to the grassroots... With the development of Guizhou’s economy and society, higher vocational medical education in Guizhou has developed rapidly, making it its mission to cultivate practical and skilled talents oriented to the grassroots and serving for frontline. However, due to the social environment, policy environment and insufficient funding, many difficulties and problems are faced. It is necessary to have a unified management throughout the province, rationally lay out higher vocational colleges and specialties, and promote the healthy and rapid development of medical higher vocational education in Guizhou with advanced concepts, proper policies, and sufficient funds in place, making higher vocational medical education in Guizhou enter a benign development period. 展开更多
关键词 HIGHER VOCATIONAL medical education in GUIZHOU Development status REFORM COUNTERMEASURE research
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