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Glomerular endothelial derived vesicles mediate podocyte dysfunction: A potential role for miRNA

N Hill1, D L Michell2, M Ramirez-Solano3

  • 1Department of Medicine, Centre for Inflammatory Disease, Imperial College London, London, United Kingdom.

Plos One
|March 28, 2020
PubMed

Insights

Glomerular endothelial cells release microRNAs (miRNA) via extracellular vesicles (EV) that impact podocyte function, contributing to kidney disease progression. This study identifies miRNA-200c-3p transfer, causing podocyte dysfunction.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • MicroRNAs (miRNA) are implicated in kidney disease pathogenesis.
  • Podocytes are crucial for glomerular filtration barrier integrity.
  • Extracellular vesicles (EV) mediate intercellular communication via miRNA transfer, but their role in regulating podocyte activity by glomerular microenvironment signals is unclear.

Purpose of the Study:

  • To investigate intercellular communication between glomerular endothelial cells (GEnC) and podocytes via EVs.
  • To characterize the impact of EV-mediated miRNA transfer on podocyte function, particularly in a disease context.

Main Methods:

  • Utilized a non-contact transwell system to model GEnC-podocyte communication in vitro.
  • Employed fluorescence cell tracking and miRNA mimetics to identify transferred EV-miRNAs.
  • Analyzed podocyte molecular profiling and functions following treatment with EVs from activated GEnC.

Main Results:

  • GEnC activation altered EV miRNA loading but not secretion.
  • EV delivery of miRNAs to podocytes modified miRNA abundance and effector functions.
  • Observed decreased VEGF secretion, increased mitochondrial stress, altered metabolism, and cytoskeletal rearrangement in podocytes.
  • Confirmed transfer of miRNA-200c-3p from activated GEnC to podocytes via EVs.

Conclusions:

  • EVs facilitate miRNA transfer from GEnCs to podocytes, influencing podocyte function.
  • miRNA-200c-3p transfer contributes to podocyte dysfunction in response to GEnC activation.
  • This mechanism highlights a novel pathway in kidney disease development.

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