机构：[1]The First People’s Hospital of Yunnan Province, Kunming, Yunnan 65000, People’s Republic of China云南省第一人民医院[2]Institute of Neuroscience, Kunming Medical University, Kunming 650031, People’s Republic of China[3]Department of Anesthesiology and Institute of Neurological Disease, State Key Lab of Biotherapy, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu 610041, People’s Republic of China四川大学华西医院[4]Molecular Imaging Laboratory, Department of Radiology, West China Hospital, Sichuan University, Chengdu 610041, People’s Republic of China四川大学华西医院[5]Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, USA[6]International Center for Spinal Cord Injury, Hugo W. Moser Research Institute at Kennedy Krieger Inc., Baltimore, MD, USA
Spinal cord injury (SCI) results in a series of severe dysfunction of sensory and motor functions, while the molecular mechanisms that cause these dysfunctions remain elusive. Using proteomics technology, Western blot (WB), and immunohistochemistry (IHC), we found endoplasmic reticulum protein 29 (ERp29) was substantially downregulated in the motor cortex 3 days postoperation (dpo) after spinal cord transection (SCT, T10) followed by a gradual recovery 28 dpo. IHC showed that ERp29 is expressed in cortical neurons. In order to investigate the role of ERp29 in axotomized cortical neurons, we developed an in vitro axotomy injury model. ERp29 overexpression in cortical neurons after axotomy protected them from apoptosis; prevented the reduction of the number of neurons, and prevented reduction of neurite length. Moreover, we found that ERp29 overexpression increased neuronal regeneration assessed by neurite number and length. Furthermore, overexpression of ERp29 in cortical neurons after axotomy increased expression of Erk-1 and PI3K while decreasing the expression of caspase-3 expression. The present data therefore provides evidence to address the role of ERp29 in axotomized cortical neurons and identifies new therapeutic targets for the treatment of SCI.
基金：
National
Natural Science Foundation of China (Grant No. 2012FB086), and
key grants from the Yunnan Science Foundation (Grant No. 2012 F001
and 2013FZ264).
第一作者机构：[1]The First People’s Hospital of Yunnan Province, Kunming, Yunnan 65000, People’s Republic of China
共同第一作者：
通讯作者：
通讯机构：[2]Institute of Neuroscience, Kunming Medical University, Kunming 650031, People’s Republic of China[3]Department of Anesthesiology and Institute of Neurological Disease, State Key Lab of Biotherapy, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu 610041, People’s Republic of China
推荐引用方式(GB/T 7714)：
Yun-Hui Zhang,Visar Belegu,Yu Zou,et al.Endoplasmic Reticulum Protein 29 Protects Axotomized Neurons from Apoptosis and Promotes Neuronal Regeneration Associated with Erk Signal[J].MOLECULAR NEUROBIOLOGY.2015,52(1):522-532.doi:10.1007/s12035-014-8840-4.
APA：
Yun-Hui Zhang,Visar Belegu,Yu Zou,Fang Wang,Bao-Jiang Qian...&Ting-Hua Wang.(2015).Endoplasmic Reticulum Protein 29 Protects Axotomized Neurons from Apoptosis and Promotes Neuronal Regeneration Associated with Erk Signal.MOLECULAR NEUROBIOLOGY,52,(1)
MLA：
Yun-Hui Zhang,et al."Endoplasmic Reticulum Protein 29 Protects Axotomized Neurons from Apoptosis and Promotes Neuronal Regeneration Associated with Erk Signal".MOLECULAR NEUROBIOLOGY 52..1(2015):522-532
