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 Ca2+ 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.
| Original language | English |
|---|---|
| Pages (from-to) | 1256-1263 |
| Number of pages | 8 |
| Journal | Environmental Toxicology and Pharmacology |
| Volume | 37 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2014 |
| Externally published | Yes |
Fingerprint
Keywords
- MARCKS
- Methylmercury
- Neurotoxicity
- Phosphorylation
ASJC Scopus subject areas
- Toxicology
- Health, Toxicology and Mutagenesis
- Pharmacology
- Medicine(all)
Cite this
Alteration in MARCKS phosphorylation and expression by methylmercury in SH-SY5Y cells and rat brain. / Shiraishi, Mitsuya; Hangai, Makoto; Yamamoto, Megumi; Sasaki, Masanori; Tanabe, Atsuhiro; Sasaki, Yasuharu; Miyamoto, Atsushi.
In: Environmental Toxicology and Pharmacology, Vol. 37, No. 3, 2014, p. 1256-1263.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Alteration in MARCKS phosphorylation and expression by methylmercury in SH-SY5Y cells and rat brain
AU - Shiraishi, Mitsuya
AU - Hangai, Makoto
AU - Yamamoto, Megumi
AU - Sasaki, Masanori
AU - Tanabe, Atsuhiro
AU - Sasaki, Yasuharu
AU - Miyamoto, Atsushi
PY - 2014
Y1 - 2014
N2 - 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 Ca2+ 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.
AB - 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 Ca2+ 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.
KW - MARCKS
KW - Methylmercury
KW - Neurotoxicity
KW - Phosphorylation
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UR - http://www.scopus.com/inward/citedby.url?scp=84900831480&partnerID=8YFLogxK
U2 - 10.1016/j.etap.2014.04.025
DO - 10.1016/j.etap.2014.04.025
M3 - Article
VL - 37
SP - 1256
EP - 1263
JO - Environmental Toxicology and Pharmacology
JF - Environmental Toxicology and Pharmacology
SN - 1382-6689
IS - 3
ER -