Phosphorylation of 14-3-3ζ at serine 58 and neurodegeneration following kainic acid-induced excitotoxicity
| Autor: | Gyeong Jae Cho, Dong Hoon Lee, Joon Soo Kim, Sang Soo Kang, Byeong Tak Jeon, Jeong Bin Kim, Gu Seob Roh, Yong Woon Cho, Wan Sung Choi, Eun Ae Jeong, Hyun Joon Kim |
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| Jazyk: | angličtina |
| Rok vydání: | 2010 |
| Předmět: |
medicine.medical_specialty
Kainic acid Pathology Programmed cell death Histology hippocampus Excitotoxicity Hippocampus Hippocampal formation medicine.disease_cause 14-3-3ζ Serine Cellular and Molecular Neuroscience chemistry.chemical_compound Neurobiology Internal medicine medicine business.industry Neurodegeneration neurodegeneration Cell Biology amygdala medicine.disease Endocrinology chemistry nervous system Phosphorylation Original Article Anatomy business Developmental Biology |
| Zdroj: | Anatomy & Cell Biology |
| ISSN: | 2093-3673 2093-3665 |
| Popis: | Oxidative stress-induced cell death leads to phosphorylation of 14-3-3ζ at serine 58. 14-3-3ζ is detected at significant levels in cerebrospinal fluid after kainic acid (KA)-induced seizures. Here we examined temporal changes in 14-3-3ζ phosphorylation in the hippocampus and amygdala of mice after KA treatment. Mice were killed at 2, 6, 24, or 48 h after KA (30 mg/kg) injection. We observed an increase in TUNEL and Fluoro-Jade B (FJB)-stained neurons in the hippocampus and amygdala of KA-treated mice. Phospho (p)-14-3-3ζ and p-JNK expression was increased in the hippocampus 2 and 6 h after KA treatment, respectively. In immunohistochemical analysis, p-14-3-3ζ-positive cells were present in the CA3 region of the hippocampus and the central nucleus of amygdala (CeA) of KA-treated mice. Thus, phosphorylation of 14-3-3ζ at serine 58 may play an important role in KA-induced hippocampal and amygdaloid neuronal damage. |
| Databáze: | OpenAIRE |
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