title: Endoplasmic Reticulum Protein 29 Protects Axotomized Neurons from Apoptosis and Promotes Neuronal Regeneration Associated with Erk Signal.
abstract: 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.
authors.affiliation: The First People's Hospital of Yunnan Province, Kunming, Yunnan, 65000, People's Republic of China.
authors.forename: Yun-Hui
authors.initials: YH
authors.lastname: Zhang
authors.forename: Visar
authors.initials: V
authors.lastname: Belegu
authors.forename: Yu
authors.initials: Y
authors.lastname: Zou
authors.forename: Fang
authors.initials: F
authors.lastname: Wang
authors.forename: Bao-Jiang
authors.initials: BJ
authors.lastname: Qian
authors.forename: Ran
authors.initials: R
authors.lastname: Liu
authors.forename: Ping
authors.initials: P
authors.lastname: Dai
authors.forename: Wei
authors.initials: W
authors.lastname: Zhao
authors.forename: Fa-Bao
authors.initials: FB
authors.lastname: Gao
authors.forename: Lei
authors.initials: L
authors.lastname: Wang
authors.forename: Li-Mei
authors.initials: LM
authors.lastname: Cao
authors.forename: John W
authors.initials: JW
authors.lastname: McDonald
authors.forename: Su
authors.initials: S
authors.lastname: Liu
authors.forename: Na
authors.initials: N
authors.lastname: Lin
authors.forename: Ting-Hua
authors.initials: TH
authors.lastname: Wang
mesh_terms: D000818:Animals; D017209:Apoptosis; D019771:Axotomy; D053148:Caspase 3 / Q000378:metabolism; D002470:Cell Survival; D002540:Cerebral Cortex / Q000378:metabolism; D015180:Electrophoresis, Gel, Two-Dimensional; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D005260:Female; D006360:Heat-Shock Proteins / Q000378:metabolism*; D020935:MAP Kinase Signaling System; D009416:Nerve Regeneration; D016501:Neurites / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D000066829:Neuroprotection; D040901:Proteomics; D017207:Rats, Sprague-Dawley; D019032:Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; D013119:Spinal Cord Injuries / Q000378:metabolism / Q000473:pathology; D013997:Time Factors
chemical_list: C110909:Erp29 protein, rat; D006360:Heat-Shock Proteins; D048049:Extracellular Signal-Regulated MAP Kinases; D053148:Caspase 3