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

研究成果: Article

4 引用 (Scopus)

抄録

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.

元の言語English
ページ(範囲)1256-1263
ページ数8
ジャーナルEnvironmental Toxicology and Pharmacology
37
発行部数3
DOI
出版物ステータスPublished - 2014
外部発表Yes

Fingerprint

Phosphorylation
Rats
Brain
Cells
Rat control
Cell death
Chelating Agents
myristoylated alanine-rich C kinase substrate
Protein Kinase C
Small Interfering RNA
Tissue

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis
  • Pharmacology
  • Medicine(all)

これを引用

Shiraishi, M., Hangai, M., Yamamoto, M., Sasaki, M., Tanabe, A., Sasaki, Y., & Miyamoto, A. (2014). Alteration in MARCKS phosphorylation and expression by methylmercury in SH-SY5Y cells and rat brain. Environmental Toxicology and Pharmacology, 37(3), 1256-1263. https://doi.org/10.1016/j.etap.2014.04.025

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.

:: Environmental Toxicology and Pharmacology, 巻 37, 番号 3, 2014, p. 1256-1263.

研究成果: Article

Shiraishi, M, Hangai, M, Yamamoto, M, Sasaki, M, Tanabe, A, Sasaki, Y & Miyamoto, A 2014, 'Alteration in MARCKS phosphorylation and expression by methylmercury in SH-SY5Y cells and rat brain', Environmental Toxicology and Pharmacology, 巻. 37, 番号 3, pp. 1256-1263. https://doi.org/10.1016/j.etap.2014.04.025
Shiraishi, Mitsuya ; Hangai, Makoto ; Yamamoto, Megumi ; Sasaki, Masanori ; Tanabe, Atsuhiro ; Sasaki, Yasuharu ; Miyamoto, Atsushi. / Alteration in MARCKS phosphorylation and expression by methylmercury in SH-SY5Y cells and rat brain. :: Environmental Toxicology and Pharmacology. 2014 ; 巻 37, 番号 3. pp. 1256-1263.
@article{07260d881fa34f8091f492b7e8ef3a3e,
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",
year = "2014",
doi = "10.1016/j.etap.2014.04.025",
language = "English",
volume = "37",
pages = "1256--1263",
journal = "Environmental Toxicology and Pharmacology",
issn = "1382-6689",
publisher = "Elsevier",
number = "3",

}

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

UR - http://www.scopus.com/inward/record.url?scp=84900831480&partnerID=8YFLogxK

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

C2 - 24835554

AN - SCOPUS:84900831480

VL - 37

SP - 1256

EP - 1263

JO - Environmental Toxicology and Pharmacology

JF - Environmental Toxicology and Pharmacology

SN - 1382-6689

IS - 3

ER -