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Cadmium induces BNIP3-dependent autophagy in chicken spleen by modulating miR-33-AMPK axis

Menghao Chen1, Xiaojing Li1, Ruifeng Fan1

  • 1College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, PR China.

Chemosphere
|December 11, 2017
PubMed

Insights

Cadmium exposure harms chicken spleen by disrupting microRNA-33-5q, leading to BNIP3-dependent autophagy via specific signaling pathways and affecting ion balance.

Area of Science:

  • Environmental toxicology
  • Molecular biology
  • Cellular signaling

Background:

  • Cadmium (Cd) is a pervasive environmental pollutant with known toxicity to organs like the spleen.
  • The precise mechanisms of Cd-induced spleen toxicity and the involvement of microRNAs (miRNAs) are not fully elucidated.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying cadmium-induced spleen toxicity in chickens.
  • To explore the role of microRNA-33-5q (miR-33-5q) in cadmium toxicity within the spleen.

Main Methods:

  • Chickens were fed cadmium chloride (CdCl2) for 90 days.
  • Techniques included electron microscopy, quantitative polymerase chain reaction (qPCR), and Western blotting.
  • Analysis of signaling pathways, autophagy markers, and ion homeostasis was performed.

Main Results:

  • Cd exposure suppressed miR-33-5q, increasing AMP-activated protein kinase (AMPK) levels.
  • This led to decreased AKT/mTOR signaling and heat shock protein 70 (HSP70), with concurrent increases in NF-κB and JNK phosphorylation.
  • Expression of BNIP3 and autophagy markers (LC3-I, LC3-II, Beclin-1) significantly increased, alongside alterations in splenic ion levels.

Conclusions:

  • Cadmium induces spleen toxicity through the deregulation of the miR-33-AMPK axis, promoting BNIP3-dependent autophagy.
  • The process involves the AKT/mTOR, HSP70-NF-κB/JNK signaling pathways, and affects ion homeostasis in the chicken spleen.
Keywords:
AutophagyCadmiumChicken spleenmicroRNA-33

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