P44/42 MAPK signal pathway-mediated hyperphosphorylation of paxillin and redistribution of E-cadherin was involved in microcystin-LR-reduced cellular adhesion in a human liver cell line

Yu Sun, Xiaomu Yu, Mo Li, Jinghui Liu

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

Microcystin-LR (MC-LR) is the most common and toxic variant of microcystins. We hypothesize that p44/42 MAPK (ERK1/2) signal pathway is involved in MC-LR-induced cell adhesion alteration in a human liver cell line-HL7702. We identified that MC-LR constantly activated MEK1/2-ERK1/2 signal pathway for 24 h, 48 h and 72 h in vitro. MC-LR reduced hepatocytes adhesion efficiency. Furthermore, as the focal adhesion biomarker, hyperphosphorylation of paxillin (ser83) was induced by MC-LR, which can be blocked by ERK1/2 pathway inhibitor (U0126) and was enhanced after hepatocytes transfected with pCMV6-MAPK plasmid. E-cadherin, as a biomarker which reflects the dynamic of cell-cell adhesion, its redistribution in hepatocytes was induced by MC-LR, and these redistribution and colocalization can be attenuated by U0126. Furthermore, MC-LR increased the co-localization efficiency of p-ERK1/2 with E-cadherin and paxillin. Finally, MC-LR-induced adhesive alteration of hepatocytes can be blocked by ERK1/2 signal pathway inhibitor. These data suggest ERK1/2-phospho-paxillin (ser83)/E-cadherin axis is involved in MC-LR toxic mechanism, which probably provides adaptive protection against MC-LR-induced hepatocytes adhesion changes.

Original languageEnglish
Pages (from-to)594-602
Number of pages9
JournalChemosphere
Volume200
DOIs
StatePublished - Jun 2018

Bibliographical note

Publisher Copyright:
© 2018 Elsevier Ltd

Keywords

  • Adhesion
  • E-cadherin
  • MAPK
  • Microcystin-LR
  • Paxillin

ASJC Scopus subject areas

  • General Chemistry
  • Public Health, Environmental and Occupational Health
  • Pollution
  • Health, Toxicology and Mutagenesis
  • Environmental Engineering
  • Environmental Chemistry

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