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作 者:Yu-Mei Feng Jian Shao Min Cai Yi-Yue Zhou Yi Yao Jia-Xi Qian Zi-Han Ding Mao-Rong Jiang Deng-Bing Yao
机构地区:[1]School of Life Sciences,Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education,Coinnovation Center of Neuroregeneration,Nantong University,Nantong,Jiangsu Province,China [2]Medical School of Nantong University,Nantong,Jiangsu Province,China [3]Nantong University Xinglin College,Nantong,Jiangsu Province,China
出 处:《Neural Regeneration Research》2023年第8期1847-1851,共5页中国神经再生研究(英文版)
基 金:supported by the National Natural Science Foundation of China,Nos.31971277(to DBY),31950410551(to DBY);Scientific Research Foundation for Returned Scholars,Ministry of Education of China(to DBY);a project funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions(PAPD)(to DBY);the Postgraduate Research&Practice Innovation Program of Jiangsu Province of China,No.KYCX 19-2050(to JS);Jiangsu College Students’Innovation and Entrepreneurship Training Program,No.202213993005Y(to YY)。
摘 要:Our previous studies have shown that long noncoding RNA(lncRNA)H19 is upregulated in injured rat sciatic nerve during the process of Wallerian degeneration,and that it promotes the migration of Schwann cells and slows down the growth of dorsal root ganglion axons.However,the mechanism by which lncRNA H19 regulates neural repair and regeneration after peripheral nerve injury remains unclear.In this study,we established a Sprague-Dawley rat model of sciatic nerve transection injury.We performed in situ hybridization and found that at 4–7 days after sciatic nerve injury,lncRNA H19 was highly expressed.At 14 days before injury,adeno-associated virus was intrathecally injected into the L4–L5 foramina to disrupt or overexpress lncRNA H19.After overexpression of lncRNA H19,the growth of newly formed axons from the sciatic nerve was inhibited,whereas myelination was enhanced.Then,we performed gait analysis and thermal pain analysis to evaluate rat behavior.We found that lncRNA H19 overexpression delayed the recovery of rat behavior function,whereas interfering with lncRNA H19 expression improved functional recovery.Finally,we examined the expression of lncRNA H19 downstream target SEMA6D,and found that after lncRNA H19 overexpression,the SEMA6D protein level was increased.These findings suggest that lncRNA H19 regulates peripheral nerve degeneration and regeneration through activating SEMA6D in injured nerves.This provides a new clue to understand the role of lncRNA H19 in peripheral nerve degeneration and regeneration.
关 键 词:adeno-associated virus dorsal root ganglion lncRNA H19 nerve degeneration nerve regeneration peripheral nerve rat sciatic nerve injury semaphorin 6D Wallerian degeneration
分 类 号:R745[医药卫生—神经病学与精神病学]
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