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Surgical procedures suppress autophagic flux in the kidney

Carolyn N Brown1, Daniel Atwood1, Deepak Pokhrel1

  • 1Division of Renal Diseases and Hypertension, University of Colorado at Denver, Aurora, CO, USA.

Cell Death & Disease
|March 6, 2021
PubMed

Insights

Sham surgery and unilateral nephrectomy (UNX) in mice cause systemic inflammation and suppress kidney autophagy. These procedures increase mammalian target of rapamycin complex 1/2 (mTORC1/2) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling, impacting research findings.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Surgical Pathology

Background:

  • Surgical models are crucial for studying kidney diseases in mice.
  • The impact of surgical procedures, including sham operations and unilateral nephrectomy (UNX), on kidney physiology remains unclear.
  • Understanding these effects is vital for accurate interpretation of experimental results.

Purpose of the Study:

  • To investigate the systemic and renal effects of sham surgery and UNX in mice.
  • To elucidate the molecular mechanisms underlying observed changes, focusing on mTORC1/2, autophagy, and ERK1/2 signaling.
  • To inform researchers about potential confounding factors introduced by surgical interventions.

Main Methods:

  • Mice underwent sham surgery or UNX.
  • Kidney and serum samples were analyzed for mTORC1/2, lysosomal genes, autophagic markers (LC3-II, p62), pro-inflammatory cytokines, and ERK1/2 activation.
  • Pharmacological inhibition of MEK1/2 with trametinib was employed.

Main Results:

  • Both sham surgery and UNX increased mTORC1/2 in the remaining kidney.
  • Genes related to lysosomal biogenesis and function were downregulated.
  • Autophagic flux was suppressed, evidenced by increased p62 and lack of LC3-II accumulation post-bafilomycin A1.
  • Systemic pro-inflammatory cytokines and renal ERK1/2 activation were significantly elevated.
  • Trametinib blocked ERK1/2 activation and reduced p62 levels.

Conclusions:

  • Sham surgery and UNX induce a systemic inflammatory response and suppress kidney autophagy via an ERK1/2-mediated pathway.
  • Researchers must consider these surgical effects when interpreting studies involving kidney disease models in mice.
  • The observed changes highlight the need for careful experimental design to distinguish disease-specific effects from procedural artifacts.

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