| Literature DB >> 27324785 |
Jie Hao1,2, Xiaoqing Chen2, Ting Fu3, Jie Liu1,2, Mingchen Yu1,2, Wei Han1,2, Shuang He4, Rong Qian1,2, Feng Zhang5.
Abstract
The VHL (Von Hippel-Lindau) gene is a tumor suppressor gene, which is best known as an E3 ubiquitin ligase that negatively regulates the hypoxia inducible factor. The inactivation of VHL gene could result in the abnormal synthesis of VHL protein, which is in contact with the development and occurrence of renal clear cell carcinoma. However, the expression and possible function of VHL in central nervous system (CNS) is still unclear. To examine the function of VHL in CNS injury and repair, we used an acute spinal cord injury (SCI) model in adult rats. Western blot analysis showed an important upregulation of VHL protein, reaching a peak at day 3 and then declined during the following days. Double immunofluorescence staining showed that VHL was co-expressed with neurons, but not with astrocytes and microglia. Moreover, we detected that active caspase-3 had co-localized with VHL in neurons after SCI. Additionally in vitro, VHL depletion, by short interfering RNA, significantly reduced neuronal apoptosis. In conclusion, these data suggested that the change of VHL protein expression was related to neuronal apoptosis after SCI.Entities:
Keywords: Apoptosis; Neuron; Spinal cord injury; Von Hippel-Lindau
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Year: 2016 PMID： 27324785 DOI： 10.1007/s11064-016-1952-7
Source DB: PubMed Journal: Neurochem Res ISSN： 0364-3190 Impact factor: 3.996