1. Transient global cerebral ischemia induces up-regulation of MLTKα in hippocampal CA1 neurons.
- Author
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Su X, Zhu CL, Shi W, Ni LC, Shen JH, and Chen J
- Subjects
- Animals, Apoptosis, Astrocytes pathology, CA1 Region, Hippocampal pathology, Caspase 3 genetics, Caspase 3 metabolism, Gene Expression, Ischemic Attack, Transient enzymology, Ischemic Attack, Transient pathology, Isoenzymes genetics, Isoenzymes metabolism, JNK Mitogen-Activated Protein Kinases genetics, JNK Mitogen-Activated Protein Kinases metabolism, MAP Kinase Kinase Kinases metabolism, Male, Microglia pathology, Neurons pathology, Rats, Rats, Wistar, Signal Transduction, Up-Regulation, Astrocytes metabolism, CA1 Region, Hippocampal metabolism, Ischemic Attack, Transient genetics, MAP Kinase Kinase Kinases genetics, Microglia metabolism, Neurons metabolism
- Abstract
MLTK (mixed-lineage kinase-like mitogen-activated protein triple kinase) is a member of the mitogen-activated protein kinase family and functioned as a mitogen activated kinase kinase kinase. MLTKα, one of the alternatively spliced forms of MLTK, could activate the c-Jun N-terminal kinase pathway, which involved in cellular stress responses and apoptosis. But the role of MLTKα in neural apoptosis was still unclear. Here, we performed a transient global cerebral ischemia model (TGCI) in adult rats and detected the dynamic changes of MLTKα in hippocampal CA1 neurons and brain cortex. We found the MLTKα expression was increased shortly after TGCI and peaked after 8 h. In spatial distribution, MLTKα was widely located in neurons rather than astrocytes and microglia. Moreover, there was a concomitant up-regulation of active caspase-3. Taken together, we hypothesized the up-regulation of MLTKα played an essential role in the apoptosis of hippocampal CA1 neurons.
- Published
- 2012
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