Mercury chloride activates c-Jun N-terminal kinase and induces c-Jun expression in LLC-PK1 cells

Masato Matsuoka, Bambang Wispriyono, Yoshihisa Iryo, Hideki Igisu

Research output: Contribution to journalArticlepeer-review

20 Citations (Scopus)

Abstract

In response to various environmental stresses including heavy metals, the c-Jun N-terminal kinase (JNK) is phosphorylated and then it phosphorylates c-Jun protein. In the present study, effects of mercury chloride (HgCl2) on JNK signalling pathway were examined in LLC-PK1 cells. When exposed to 10 or 20 μM HgCl2, the level of phosphorylated JNK and the activity of JNK assayed in vitro using glutathione-S-transferase-c-Jun as substrate increased markedly. The level of phosphorylated JNK increased 30 min after HgCl2 exposure and remained elevated even at 8 h. On the other hand, no changes were found in the total amount of JNK protein. Consistent with the activation of JNK, c-Jun proteins phosphorylated on Ser63 and Ser73 were accumulated in cells exposed to HgCl2. Concomitantly, the levels of c- jun mRNA and c-Jun protein were elevated. When compared to other heavy metal compounds such as manganese chloride, zinc chloride, cadmium chloride, and lead chloride, HgCl2 could phosphorylate JNK more markedly. Neither intracellular Ca2+ nor sulfhydryl groups appeared to play a major role in the activation of JNK by HgCl2 exposure in this porcine renal epithelial cell line.

Original languageEnglish
Pages (from-to)361-368
Number of pages8
JournalToxicological Sciences
Volume53
Issue number2
Publication statusPublished - 28 Feb 2000

Keywords

  • c-jun
  • c-Jun N-terminal kinase
  • c-Jun protein
  • LLC-PK cells
  • Mercury chloride
  • Nephrotoxicity

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