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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Shiraishi, Mitsuya Hangai, Makoto Yamamoto, Megumi Sasaki, Masanori Tanabe, Atsuhiro Sasaki, Yasuharu Miyamoto, Atsushi |
| Description | Author Affiliation: Shiraishi M ( Department of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Kagoshima University, 1-21-24 Korimoto, Kagoshima 890-0065, Japan. Electronic address: shira-m@vet.kagoshima-u.ac.jp.); Hangai M ( Department of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Kagoshima University, 1-21-24 Korimoto, Kagoshima 890-0065, Japan.); Yamamoto M ( Department of Basic Medical Sciences, National Institute for Minamata Disease, 4058-18 Hama, Minamata, Kumamoto 867-0008, Japan.); Sasaki M ( Department of Basic Medical Sciences, National Institute for Minamata Disease, 4058-18 Hama, Minamata, Kumamoto 867-0008, Japan.); Tanabe A ( Department of Bioscience and Engineering, College of Systems Engineering and Science, Shibaura Institute of Technology, 307 Fukasaku, Minuma-ku, Saitama 337-8570, Japan.); Sasaki Y ( Laboratory of Pharmacology, School of Pharmaceutical Science, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo 108-8641, Japan.); Miyamoto A ( Department of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Kagoshima University, 1-21-24 Korimoto, Kagoshima 890-0065, Japan.) |
| Abstract | The molecular mechanisms mediating methylmercury (MeHg)-induced neurotoxicity are not completely understood. Because myristoylated alanine-rich C kinase substrate (MARCKS) plays an essential role in the differentiation and development of neuronal cells, we studied the alteration of MARCKS expression and phosphorylation in MeHg-induced neurotoxicity of neuroblastoma SH-SY5Y cells and in the rat brain. Exposure to MeHg induced a decrease in cell viability of SH-SY5Y cells, which was accompanied by a significant increase in phosphorylation and a reduction in MARCKS expression. Pretreatment of cells with a protein kinase C inhibitor or an extracellular Ca(2+) chelator suppressed MeHg-induced MARCKS phosphorylation. In MARCKS knock-down cells, MeHg-induced cell death was significantly augmented in comparison to control siRNA. In brain tissue from MeHg-treated rats, MARCKS phosphorylation was enhanced in the olfactory bulb in comparison to control rats. The present study may indicate that alteration in MARCKS expression or phosphorylation has consequences for MeHg-induced neurotoxicity. |
| File Format | HTM / HTML |
| ISSN | 13826689 |
| Issue Number | 3 |
| Volume Number | 37 |
| e-ISSN | 18727077 |
| Journal | Environmental Toxicology and Pharmacology |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2014-05-01 |
| Publisher Place | Netherlands |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Environmental Health Discipline Pharmacology Brain Drug Effects Intracellular Signaling Peptides And Proteins Metabolism Membrane Proteins Methylmercury Compounds Toxicity Neurotoxins Animals Cell Line, Tumor Cell Survival Humans Male Phosphorylation Rats, Wistar Journal Article Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Health, Toxicology and Mutagenesis Medicine Toxicology Pharmacology |
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