当前位置: 首页 > 详情页

TRIM32 affects the recovery of motor function following spinal cord injury through regulating proliferation of glia

文献详情

资源类型:

收录情况: ◇ SCIE

机构: [1]Affiliated Bayi Brain Hospital, P.L.A. Army General Hospital, Beijing 100700, China [2]Department of Neurosurgery, The 251st Hospital of P.L.A., Zhangjiakou 075000, China [3]Third Military Medical University, Chongqing 400038, China [4]Southern Medical University, Guangzhou 510515, China [5]School of Nursing, Binzhou Medical University, Yantai 264000, China [6]Institute of Neuroscience and Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou 215021, China [7]Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China
出处:
ISSN:

关键词: spinal cord injury tripartite motif protein 32 axonal regeneration glia neuroinflammation

摘要:
Both the extrinsic environmental factors and intrinsic neuronal mechanisms limit the axonal regeneration after spinal cord injury (SCI). However, the underlying molecular mechanisms remain unclear. In the present study, we identify tripartite motif protein 32 (TRIM32), an E3 ubiquitin ligase, which is barely detected in glial cells in the normal uninjured spinal cord, exhibits strong expression in both astrocytes and microglia following SCI. We further observe that deficiency of TRIM32 results in increased numbers of astrocytes and microglia, which is accompanied by enhanced proliferation of both cells and increased secretion of interleukin (IL)-1 and IL-10. The axonal regeneration is impaired in the spinal cord of TRIM32(-/-)mice following SCI, which is indicated by increased distances of the corticospinal tracts (CST) fiber to the lesion site and less axonal sprouting. We further show that deficiency of TRIM32 results in delay motor recovery following SCI. Therefore, TRIM32 is a novel essential positive factor modulating axonal regeneration and the recovery of motor function following SCI, possibly through suppressing proliferation of glial cells.

基金:
语种:
被引次数:
WOS:
PubmedID:
中科院(CAS)分区:
出版当年[2016]版:
大类 | 1 区 医学
小类 | 2 区 细胞生物学 2 区 肿瘤学
最新[2023]版:
JCR分区:
出版当年[2015]版:
Q1 CELL BIOLOGY Q1 ONCOLOGY
最新[2023]版:

影响因子: 最新[2023版] 最新五年平均 出版当年[2015版] 出版当年五年平均 出版前一年[2014版] 出版后一年[2016版]

第一作者:
第一作者机构: [1]Affiliated Bayi Brain Hospital, P.L.A. Army General Hospital, Beijing 100700, China [2]Department of Neurosurgery, The 251st Hospital of P.L.A., Zhangjiakou 075000, China
共同第一作者:
通讯作者:
通讯机构: [1]Affiliated Bayi Brain Hospital, P.L.A. Army General Hospital, Beijing 100700, China [3]Third Military Medical University, Chongqing 400038, China [4]Southern Medical University, Guangzhou 510515, China [6]Institute of Neuroscience and Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou 215021, China [7]Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China
推荐引用方式(GB/T 7714):
APA:
MLA:

资源点击量:16409 今日访问量:0 总访问量:869 更新日期:2025-01-01 建议使用谷歌、火狐浏览器 常见问题

版权所有©2020 首都医科大学宣武医院 技术支持:重庆聚合科技有限公司 地址:北京市西城区长椿街45号宣武医院