Short‐term, low‐dose cadmium exposure induces hyperpermeability in human renal glomerular endothelial cells. Issue 2 (25th May 2015)

• Record Type: Journal Article
• Authors: Li, Liqun; Dong, Fengyun; Xu, Dongmei; Du, Linna; Yan, Suhua; Hu, Hesheng; Lobe, Corrinne G.; Yi, Fan; Kapron, Carolyn M.; Liu, Ju
• Is Part Of: Journal of applied toxicology. Volume 36:Issue 2(2016)
• Page Start: 257
• Page End: 265
• Publication Date: 2015-05-25
• Subjects: cadmium -- renal glomerular endothelial cells -- permeability -- VE‐cadherin -- p38 MAPK; Toxicology -- Periodicals; Industrial toxicology -- Periodicals; Environmentally induced diseases -- Periodicals; Toxicology -- Periodicals; 615.9005
• DOI: 10.1002/jat.3168
• Languages: English
• ISSNs: 0260-437X

Abstract

Abstract: The kidney is the principal organ targeted by exposure to cadmium (Cd), a well‐known toxic metal. Even at a low level, Cd damages glomerular filtration. However, little is known about the effects of Cd on the glomerular endothelium, which performs the filtration function and directly interacts with Cd in blood plasma. In this study, we cultured human renal glomerular endothelial cells (HRGECs) in the presence of serum with treatment of a short term (1 h) and low concentration (1 μ m) of Cd, which mimics the pattern of glomerular endothelium exposure to Cd in vivo . We found that this short‐term, low‐dose Cd exposure does not induce cytotoxicity, but increases permeability in HRGECs monolayers and redistributes adherens junction proteins vascular endothelial‐cadherin and β‐catenin. Though short‐term, low‐dose Cd exposure activates all three major mitogen activated protein kinases, only the inhibitor of p38 mitogen activated protein kinase partially prevents Cd‐induced hyperpermeability in HRGECs. Our data indicate that the presence of Cd in blood circulation might directly disrupt the glomerular endothelial cell barrier and contribute to the development of clinical symptoms of glomerular diseases. Copyright © 2015 John Wiley & Sons, Ltd. Abstract : Cadmium enters the human body and circulates for a short period in the bloodstream. In this study, we found that short‐term, low‐dose cadmium exposure increases permeability without cytotoxic effects in human renal glomerular endothelial cells. The hyperpermeability might be caused by membrane dissociation of vascular endothelial cadherin and is partially mediated by p38 mitogen‐activated protein kinase pathway.