Imperial College London

DrNeilHill

Faculty of MedicineDepartment of Metabolism, Digestion and Reproduction

Honorary Clinical Senior Lecturer
 
 
 
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Contact

 

n.hill

 
 
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Location

 

East WingCharing Cross Campus

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Summary

 

Publications

Citation

BibTex format

@article{Hill:2020:10.1371/journal.pone.0224852,
author = {Hill, N and Michell, DL and Ramirez-Solano, M and Sheng, Q and Pusey, C and Vickers, KC and Woollard, KJ},
doi = {10.1371/journal.pone.0224852},
journal = {PLoS One},
title = {Glomerular endothelial derived vesicles mediate podocyte dysfunction: A potential role for miRNA},
url = {http://dx.doi.org/10.1371/journal.pone.0224852},
volume = {15},
year = {2020}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - MicroRNAs (miRNA) are shown to be involved in the progression of several types of kidney diseases. Podocytes maintain the integrity of the glomerular basement membrane. Extracellular vesicles (EV) are important in cell-to-cell communication as they can transfer cellular content between cells, including miRNA. However, little is known about how extracellular signals from the glomerular microenvironment regulate podocyte activity. Using a non-contact transwell system, communication between glomerular endothelial cells (GEnC) and podocytes was characterised in-vitro. Identification of transferred EV-miRNAs from GEnC to podocytes was performed using fluorescence cell tracking and miRNA mimetics. To represent kidney disease, podocyte molecular profiling and functions were analysed after EV treatments derived from steady state or activated GEnC. Our data shows activation of GEnC alters EV-miRNA loading, but activation was not found to alter EV secretion. EV delivery of miRNA to recipient podocytes altered cellular miRNA abundance and effector functions in podocytes, including decreased secretion of VEGF and increased mitochondrial stress which lead to altered cellular metabolism and cytoskeletal rearrangement. Finally, results support our hypothesis that miRNA-200c-3p is transfered by EVs from GEnC to podocytes in response to activation, ultimately leading to podocyte dysfunction.
AU - Hill,N
AU - Michell,DL
AU - Ramirez-Solano,M
AU - Sheng,Q
AU - Pusey,C
AU - Vickers,KC
AU - Woollard,KJ
DO - 10.1371/journal.pone.0224852
PY - 2020///
SN - 1932-6203
TI - Glomerular endothelial derived vesicles mediate podocyte dysfunction: A potential role for miRNA
T2 - PLoS One
UR - http://dx.doi.org/10.1371/journal.pone.0224852
UR - https://www.ncbi.nlm.nih.gov/pubmed/32214346
UR - http://hdl.handle.net/10044/1/78795
VL - 15
ER -