siRNA-mediated AMPK.ALPHA.1 subunit gene PRKAA1 silencing enhances methylmercury toxicity in HEK293 cells

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  • Hwang Gi-Wook
    Laboratory of Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University
  • Tobita Mayumi
    Laboratory of Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University
  • Takahashi Tsutomu
    Laboratory of Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University
  • Kuge Shusuke
    Laboratory of Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University Department of Microbiology, Tohoku Pharmaceutical University
  • Kita Kayoko
    Laboratory of Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University Laboratory of Toxicology, Faculty of Pharmaceutical Sciences, Teikyo University
  • Naganuma Akira
    Laboratory of Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University

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  • Toxicogenomics/proteomics report: siRNA-mediated AMPKα1 subunit gene PRKAA1 silencing enhances methylmercury toxicity in HEK293 cells
  • Toxicogenomics proteomics report siRNA mediated AMPK a1 subunit gene PRKAA1 silencing enhances methylmercury toxicity in HEK293 cells

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The environmental pollutant methylmercury is a potent neurotoxin. The mechanisms of toxicity and biological defense remain largely unknown. We found that inhibiting the expression of PRKAA1 (AMPKα1), an activated subunit of AMP-activated protein kinase (AMPK), increased susceptibility of HEK293 cells to methylmercury toxicity. Treatment of the cells with AICAR (5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside), an AMPK activator, reduced the methylmercury toxicity. Here, we suggest for the first time that the activation (phosphorylation) of AMPK may play an important role in reducing the toxicity of methylmercury.

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