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

Xiaocui Chen, Jing Li, Zuowang Cheng, Yinghua Xu, Xia Wang, Xiaorui Li, Dongmei Xu, Carolyn M. Kapron and Ju Liu
Additional contact information
Xiaocui Chen: Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, 16766 Jingshi Road, Jinan 250014, China
Jing Li: Key Laboratory of Molecular and Nano Probes, Ministry of Education, College of Chemistry, Chemical Engineering and Materials Science, Shandong Normal University, Jinan 250014, China
Zuowang Cheng: Taishan Medical College, Taian 271000, China
Yinghua Xu: Taishan Medical College, Taian 271000, China
Xia Wang: Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, 16766 Jingshi Road, Jinan 250014, China
Xiaorui Li: Taishan Medical College, Taian 271000, China
Dongmei Xu: Department of Nephrology, Shandong Provincial Qianfoshan Hospital, Shandong University, 16766 Jingshi Road, Jinan 250014, China
Carolyn M. Kapron: Department of Biology, Trent University, Peterborough, ON K9L0G2, Canada
Ju Liu: Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, 16766 Jingshi Road, Jinan 250014, China

IJERPH, 2016, vol. 13, issue 10, 1-12

Abstract: 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 ?M 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 ?-smooth muscle actin and platelet-derived growth factor receptor-?, 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.

Keywords: cadmium; renal mesangial cells; JNK pathway; proliferation (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2016
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.mdpi.com/1660-4601/13/10/990/pdf (application/pdf)
https://www.mdpi.com/1660-4601/13/10/990/ (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:gam:jijerp:v:13:y:2016:i:10:p:990-:d:79897

Access Statistics for this article

IJERPH is currently edited by Ms. Jenna Liu

More articles in IJERPH from MDPI
Bibliographic data for series maintained by MDPI Indexing Manager ().