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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
Summary
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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