Skip to main content

ETHNOS_APP

Home • Search • Journals • List 0

Low Dose Cadmium Inhibits Proliferation of Human Renal Mesangial Cells via Activation of the JNK Pathway

Bibliographic Data

ID15501882
AuthorsXiaocui Chen (0009-0002-4927-390X, Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, 16766 Jingshi Road, Jinan 250014, China), Jiayao Chen (0000-0001-6749-8358, Shandong University), Jing Li (0000-0001-7792-4322, Shandong Normal University), Zuowang Cheng (Taishan Medical University), Yinghua Xu (0000-0003-0148-0184, Taishan Medical University), Xia Wang (0000-0002-5256-0611, Shandong University), Xiaorui Li (0000-0002-0627-3101, Taishan Medical University), Dongmei Xu (0000-0002-8192-1535, Shandong University), Carolyn Kapron (0000-0001-8630-8214, Trent University), Ju Liu (0000-0002-1352-1986, Shandong University, corresponding author)
Year2016
Volume13
Issue10
Pages990-990
Publication date2016-10-07
Peer ReviewedYes
Open AccessYes
TypeARTICLE
VenueInternational Journal of Environmental Research and Public Health (JOURNAL)
Journal identifiersISSN: 1661-7827 • E-ISSN: 1660-4601
PublisherMultidisciplinary Digital Publishing Institute (PUBLISHER • CH)
DOI10.3390/ijerph13100990
PMID27739415
OpenAlexW2528104714
LanguageEN
References cited52

Cadmium (Cd) is a heavy metal and environmental pollutant. The kidney is the principal target organ of Cd exposure. Previously, we found that low concentration of Cd damages the integrity of the glomerular filtration barrier. However, little is known about the effects of Cd on renal mesangial cells, which provide structural support for the glomerular capillary loops and regulate intraglomerular blood flow. In this study, human renal mesangial cells (HRMCs) were cultured in the presence of serum and treated with 4 μM Cd. We found that Cd activates the c-Jun N-terminal kinase (JNK) pathway, and increases the protein levels of c-Jun and c-Fos. Cd treatment also induces a decrease in proliferation and an increase in apoptosis of HRMCs, but only the decrease in HRMC proliferation was reversed by pretreatment with SP600125, an inhibitor of the JNK pathway. In addition, Cd does not change the expression of α-smooth muscle actin and platelet-derived growth factor receptor-β, the markers of mesangial cells, or the alignment of the filamentous actin (F-actin) cytoskeleton of HRMCs. Our data indicate that the JNK pathway mediates the inhibitory effects of Cd on HRMC proliferation

Actin · Actin cytoskeleton · Apoptosis · Biology · c-jun · Cell · Cell growth · Cytoskeleton · Kidney · Mesangial cell · Signal transduction · Transcription factor · Chemistry · Heavy Metal Exposure and Toxicity · Medicine · Mercury impact and mitigation studies · Biochemistry · Cell Biology · Endocrinology · Internal Medicine

  • Low-Dose Cadmium Upregulates Vegf Expression in Lung Adenocarcinoma Cells

    Open Access•Fuhong Liu, Bei Wang et al.•International Journal of…•2015

Citation velocityhistorical
Highly citedNo

Tools

Open DOISci-HubOpen Access
Ethnos_APP • Open Source Project • MIT License • Frontend v2.0.0 • Privacy and Cookies • API Documentation: api.ethnos.app/docs • API Source Code: GitHub • DOI: 10.5281/zenodo.17049435 • Frontend Source Code: GitHub • DOI: 10.5281/zenodo.17050053 • cruz.rio.br • Expectantes Misericordiae