Exosomes from high glucose-treated glomerular endothelial cells activate mesangial cells to promote renal fibrosis

The interaction between glomerular endothelial cells (GECs) and glomerular mesangial cells (GMCs) is an essential aspect of diabetic nephropathy (DN). Therefore, understanding how GECs communicate with GMCs in the diabetic environment is crucial for the development of new targets for the prevention...

Full description

Saved in:
Bibliographic Details
Published in:Biology open 2016-04, Vol.5 (4), p.484-491
Main Authors: Wu, Xiao-Ming, Gao, Yan-Bin, Cui, Fang-Qiang, Zhang, Na
Format: Article
Language:English
Subjects:
Actin
Activation
Cell interactions
Diabetes mellitus
Endothelial cells
Exosome
Exosomes
Extracellular matrix
Fibrosis
Glomerular endothelial cells
Glomerular mesangial cells
Glucose
High glucose
Matrix protein
Membrane vesicles
Mesangial cells
miRNA
mRNA
Muscles
Nephropathy
Pathogenesis
Proteins
Renal Fibrosis
Ribonucleic acid
RNA
Signal transduction
Smad3 protein
Smooth muscle
Transforming growth factor-b1
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The interaction between glomerular endothelial cells (GECs) and glomerular mesangial cells (GMCs) is an essential aspect of diabetic nephropathy (DN). Therefore, understanding how GECs communicate with GMCs in the diabetic environment is crucial for the development of new targets for the prevention and treatment of DN. Exosomes, nanometer-sized extracellular membrane vesicles secreted by various cell types, play important roles in cell-to-cell communication via the transfer of mRNA, microRNA and protein. In this study, we demonstrate that high glucose (HG)-treated GECs secrete a higher number of exosomes highly enriched in TGF-β1 mRNA compared with normal glucose (NG)-treated GECs. Exosomes released by HG-treated GECs can promote α-smooth muscle actin (α-SMA) expression, proliferation and extracellular matrix protein overproduction in GMCs through the TGF-β1/Smad3 signaling pathway. Thus, we provide new insights into the pathogenesis of DN that involves intercellular transfer of TGF-β1 mRNA in the GEC-to-GMC direction via exosomes.
ISSN:2046-6390
2046-6390
DOI:10.1242/bio.015990