Up-regulation of NFATc4 involves in neuronal apoptosis following intracerebral hemorrhage
Autor: | Kaifu Ke, Maohong Cao, Heyi Zheng, Ying Rui, Peipei Zhai, Jiabing Shen, Ling Xu, Lei Li, Jianghua Zhao, Wei Xu, Xiang Tan, Tingting Zhai |
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Rok vydání: | 2013 |
Předmět: |
Male
Time Factors Blotting Western Fluorescent Antibody Technique Apoptosis Nerve Tissue Proteins Biology PC12 Cells Fas ligand Rats Sprague-Dawley Cellular and Molecular Neuroscience Downregulation and upregulation Western blot RNA interference medicine Animals Cerebral Hemorrhage Intracerebral hemorrhage Neurons medicine.diagnostic_test Behavior Animal NFATC Transcription Factors Caspase 3 Cell Biology General Medicine medicine.disease Immunohistochemistry Cell biology Rats Up-Regulation Blot medicine.anatomical_structure Phenotype Neuron Neuroscience |
Zdroj: | Cellular and molecular neurobiology. 33(7) |
ISSN: | 1573-6830 |
Popis: | Nuclear factor of activated T-cells, cytoplasmic 4 (NFATc4), a transcriptional factor, is involved in the control about the flow of genetic information and the modulation of diverse cellular activities. Accumulating evidence has demonstrated that NFATc4 exerted a pro-apoptotic effect in multiple diseases. Here, we explored the NFATc4’s roles during the pathophysiological processes of intracerebral hemorrhage (ICH). An ICH rat model was built and evaluated according to behavioral testing. Using Western blot, immunohistochemistry, and immunofluorescence, significant up-regulation of NFATc4 was found in neurons in brain areas surrounding the hematoma following ICH. Increasing NFATc4 expression was found to be accompanied by the up-regulation of Fas ligand (FasL), active caspase-8, and active caspase-3, respectively. Besides, NFATc4 co-localized with active caspase-3 in neurons, indicating its role in neuronal apoptosis. Our in vitro study, using NFATc4 RNA interference in PC12 cells, further confirmed that NFATc4 might exert its pro-apoptotic function in neuronal apoptosis through extrinsic pathway. Thus, NFATc4 may play a role in promoting the brain secondary damage following ICH. |
Databáze: | OpenAIRE |
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