Endoplasmic Reticulum Protein 29 Protects Axotomized Neurons from Apoptosis and Promotes Neuronal Regeneration Associated with Erk Signal

Yun Hui Zhang, Visar Belegu, Yu Zou, Fang Wang, Bao Jiang Qian, Ran Liu, Ping Dai, Wei Zhao, Fa Bao Gao, Lei Wang, Li Mei Cao, John W. McDonald, Su Liu, Na Lin, Ting Hua Wang

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)522-532
Number of pages11
JournalMolecular Neurobiology
Volume52
Issue number1
DOIs
StatePublished - Aug 25 2015

Keywords

  • Apoptosis
  • Axotomy
  • Cortical neurons
  • ERp29
  • Erk signaling
  • Neuronal regeneration
  • SCT

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience

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