Alteration in MARCKS phosphorylation and expression by methylmercury in SH-SY5Y cells and rat brain

Mitsuya Shiraishi; Makoto Hangai; Megumi Yamamoto; Masanori Sasaki; Atsuhiro Tanabe; Yasuharu Sasaki; Atsushi Miyamoto

doi:10.1016/j.etap.2014.04.025

Alteration in MARCKS phosphorylation and expression by methylmercury in SH-SY5Y cells and rat brain

Mitsuya Shiraishi, Makoto Hangai, Megumi Yamamoto, Masanori Sasaki, Atsuhiro Tanabe, Yasuharu Sasaki, Atsushi Miyamoto

Research output: Contribution to journal › Article › peer-review

5 Citations (Scopus)

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	https://doi.org/10.1016/j.etap.2014.04.025
Publication status	Published - 2014 May

Keywords

MARCKS
Methylmercury
Neurotoxicity
Phosphorylation

ASJC Scopus subject areas

Toxicology
Pharmacology
Health, Toxicology and Mutagenesis

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10.1016/j.etap.2014.04.025

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title = "Alteration in MARCKS phosphorylation and expression by methylmercury in SH-SY5Y cells and rat brain",

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.",

keywords = "MARCKS, Methylmercury, Neurotoxicity, Phosphorylation",

author = "Mitsuya Shiraishi and Makoto Hangai and Megumi Yamamoto and Masanori Sasaki and Atsuhiro Tanabe and Yasuharu Sasaki and Atsushi Miyamoto",

note = "Funding Information: This work was supported by a Grant-in-Aid for Young Scientists (B) (Grant Number 23780298 ) from the Japan Society for the Promotion of Sciences , and partly through a grant of Long-range Research Initiative (LRI) by the Japan Chemical Industry Association (JCIA).",

year = "2014",

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language = "English",

volume = "37",

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journal = "Environmental Toxicology and Pharmacology",

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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

N1 - Funding Information: This work was supported by a Grant-in-Aid for Young Scientists (B) (Grant Number 23780298 ) from the Japan Society for the Promotion of Sciences , and partly through a grant of Long-range Research Initiative (LRI) by the Japan Chemical Industry Association (JCIA).

PY - 2014/5

Y1 - 2014/5

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.

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KW - Neurotoxicity

KW - Phosphorylation

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Alteration in MARCKS phosphorylation and expression by methylmercury in SH-SY5Y cells and rat brain

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