Induction of chemokine CCL3 by NF-κB reduces methylmercury toxicity in C17.2 mouse neural stem cells

Tsutomu Takahashi, Min Seok Kim, Miyuki Iwai-Shimada, Takayuki Hoshi, Masatake Fujimura, Takashi Toyama, Yasuyuki Fujiwara, Akira Naganuma, Gi Wook Hwang

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


Methylmercury is an environmental pollutant that shows selective toxicity to the central nervous system. We previously reported that brain-specific expression of chemokine CCL3 increases in mice administered methylmercury. However, the relationship between CCL3 and methylmercury toxicity has not been elucidated. Here, we confirmed that induction of CCL3 expression occurs before pathological change by methylmercury treatment was observed in the mouse brain. This induction was also observed in C17.2 mouse neural stem cells before methylmercury-induced cytotoxicity. In addition, cells in which CCL3 was knocked-down showed higher methylmercury sensitivity than did control cells. Moreover, activation of transcription factor NF-κB was observed following methylmercury treatment, and methylmercury-mediated induction of CCL3 expression was partially suppressed by knockdown of p65, an NF-κB subunit. Our results suggest that NF-κB plays a role in the induction of methylmercury-mediated CCL3 expression and that this action may be a cellular response to methylmercury toxicity.

Original languageEnglish
Article number103216
JournalEnvironmental Toxicology and Pharmacology
Publication statusPublished - 2019 Oct


  • CCL3
  • Methylmercury
  • p65
  • Toxicity


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