Journal
TOXICOLOGY RESEARCH
Volume 9, Issue 5, Pages 683-692Publisher
OXFORD UNIV PRESS
DOI: 10.1093/toxres/tfaa067
Keywords
manganese; glomerular endothelial cells; VE-cadherin; adherens junction; glomerular filtration barrier
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Funding
- Medical Science and Technology Development Plan of Shandong Province [2018WS260]
- Natural Science Foundation of Shandong Province [ZR2019BH007]
- National Natural Science Foundation of China [81472933, 81972989, 81970615]
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Manganese (Mn) is an essential micronutrient. However, it is well established that Mn overexposure causes nervous system diseases. In contrast, there are few reports on the effects of Mn exposure on glomerular endothelium. In the present study, the potential effects of Mn exposure on glomerular endothelium were evaluated. Sprague Dawley rats were used as a model of Mn overexposure by intraperitoneal injection of MnCl2 center dot H2O at 25 mg/kg body weight. Mn exposure decreased expression of vascular endothelial-cadherin, a key component of adherens junctions, and increased exudate from glomeruli in Sprague Dawley rats. Human renal glomerular endothelial cells were cultured with different concentration of Mn. Exposure to 0.2 nM Mn increased permeability of human renal glomerular endothelial cell monolayers and decreased vascular endothelial-cadherin expression without inducing cytotoxicity. In addition, Mn exposure increased phosphorylation of mothers against decapentaplegic homolog 2/3 and upregulated expression of zinc finger protein SNAI1, a negative transcriptional regulator of vascular endothelial-cadherin. Our data suggest Mn exposure may contribute to development of glomerular diseases by inducing permeability of glomerular endothelium. [GRAPHICS] .
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