Upregulation of 3-MST Relates to Neuronal Autophagy After Traumatic Brain Injury in Mice
详细信息 查看全文
- 作者：Mingyang Zhang ; Haiyan Shan ; Pan Chang ; Lu Ma…
- 关键词：3 ; mercaptopyruvate sulfurtransferase ; Traumatic brain injury ; Autophagic cell death ; Mice
- 刊名：Cellular and Molecular Neurobiology
- 出版年：2017
- 出版时间：March 2017
- 年：2017
- 卷：37
- 期：2
- 页码：291-302
- 全文大小：
- 刊物类别：Biomedical and Life Sciences
- 刊物主题：Neurosciences; Cell Biology; Neurobiology;
- 出版者：Springer US
- ISSN：1573-6830
- 卷排序：37
文摘
3-mercaptopyruvate sulfurtransferase (3-MST) was a novel hydrogen sulfide (H2S)-synthesizing enzyme that may be involved in cyanide degradation and in thiosulfate biosynthesis. Over recent years, considerable attention has been focused on the biochemistry and molecular biology of H2S-synthesizing enzyme. In contrast, there have been few concerted attempts to investigate the changes in the expression of the H2S-synthesizing enzymes with disease states. To investigate the changes of 3-MST after traumatic brain injury (TBI) and its possible role, mice TBI model was established by controlled cortical impact system, and the expression and cellular localization of 3-MST after TBI was investigated in the present study. Western blot analysis revealed that 3-MST was present in normal mice brain cortex. It gradually increased, reached a peak on the first day after TBI, and then reached a valley on the third day. Importantly, 3-MST was colocalized with neuron. In addition, Western blot detection showed that the first day post injury was also the autophagic peak indicated by the elevated expression of LC3. Importantly, immunohistochemistry analysis revealed that injury-induced expression of 3-MST was partly colabeled by LC3. However, there was no colocalization of 3-MST with propidium iodide (cell death marker) and LC3 positive cells were partly colocalized with propidium iodide. These data suggested that 3-MST was mainly located in living neurons and may be implicated in the autophagy of neuron and involved in the pathophysiology of brain after TBI.