TRIM32 affects the recovery of motor function following spinal cord injury through regulating proliferation of glia
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Qiang Fu1,2,*, Ming-Ming Zou1,3,*, Jian-Wei Zhu1,4, Yan Zhang1, Wen-Jin Chen1,4, Mei Cheng5, Chun-Feng Liu6,7, Quan-Hong Ma1,6,7, Ru-Xiang Xu1,3,4
1Affiliated Bayi Brain Hospital, P.L.A. Army General Hospital, Beijing 100700, China
2Department of Neurosurgery, The 251st Hospital of P.L.A., Zhangjiakou 075000, China
3Third Military Medical University, Chongqing 400038, China
4Southern Medical University, Guangzhou 510515, China
5School of Nursing, Binzhou Medical University, Yantai 264000, China
6Institute of Neuroscience and Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou 215021, China
7Department of Neurology and Suzhou Clinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University, Suzhou 215004, China
*These authors contributed equally to this work
Ru-Xiang Xu, email: [email protected]
Quan-Hong Ma, email: [email protected]
Keywords: spinal cord injury, tripartite motif protein 32, axonal regeneration, glia, neuroinflammation
Received: February 21, 2017 Accepted: April 15, 2017 Published: April 27, 2017
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.
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