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Involvement of MAPK/ERK1/2 pathway in microcystin-induced microfilament reorganization in HL7702 hepatocytes

Fei Yang1,2,3, Cong Wen1, Shuilin Zheng1

  • 1a Department of Occupational and Environmental Health, Xiangya School of Public Health , Central South University , Changsha , China.

Journal of Toxicology and Environmental Health. Part A
|November 14, 2018
PubMed

Insights

Microcystin-LR (MC-LR) causes liver cell damage by disrupting actin filaments and altering microRNA-451a (miR-451a) levels. This toxin impairs cellular repair mechanisms, even when miR-451a is supplemented.

Area of Science:

  • Hepatotoxicity and cellular damage mechanisms
  • Molecular biology and microRNA regulation
  • Environmental toxicology and cyanotoxins

Background:

  • Microcystin-LR (MC-LR) is a potent cyanotoxin known to induce cytoskeletal damage, particularly affecting actin filaments.
  • The precise molecular mechanisms underlying MC-LR-induced cytoskeletal reorganization remain incompletely understood.
  • MicroRNA-451a (miR-451a) is a critical regulator of cellular processes, including proliferation, apoptosis, and tumorigenesis.

Purpose of the Study:

  • To investigate the impact of MC-LR on microfilament depolarization in HL7702 liver cells.
  • To assess the effect of MC-LR on the expression levels of miR-451a.
  • To elucidate the relationship between MC-LR exposure, miR-451a expression, and key signaling pathways.

Main Methods:

  • HL7702 liver cells were treated with 5 or 10 µM MC-LR for 24 hours.
  • Microfilament depolarization was assessed.
  • Expression levels of miR-451a, phosphorylation of MAPK/ERK1/2 and VASP were measured.
  • Total ERK1/2 protein levels were analyzed.
  • The efficacy of miR-451a transfection in mitigating MC-LR effects on PP1 and PP2A was evaluated.

Main Results:

  • MC-LR exposure led to increased microfilament depolarization.
  • Phosphorylation of MAPK/ERK1/2 and VASP was elevated, while total ERK1/2 remained unchanged.
  • MC-LR significantly decreased miR-451a RNA expression levels.
  • Overexpression of miR-451a did not prevent MC-LR-induced inhibition of protein phosphatases PP1 and PP2A or cytoskeletal disruption.

Conclusions:

  • MC-LR induces cytoskeletal damage in liver cells through mechanisms involving microfilament depolarization and altered signaling pathways.
  • MC-LR exposure downregulates miR-451a expression.
  • Therapeutic strategies involving miR-451a supplementation may be ineffective in counteracting MC-LR toxicity due to interference with essential cellular processes.
Keywords:
HepatocytesMAPK/ERK1/2Microcystin-LRMicrofilamentToxicity

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