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

Author

Listed:
  • 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)

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 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.

Suggested Citation

  • Xiaocui Chen & Jing Li & Zuowang Cheng & Yinghua Xu & Xia Wang & Xiaorui Li & Dongmei Xu & Carolyn M. Kapron & Ju Liu, 2016. "Low Dose Cadmium Inhibits Proliferation of Human Renal Mesangial Cells via Activation of the JNK Pathway," IJERPH, MDPI, vol. 13(10), pages 1-12, October.
    • Handle: RePEc:gam:jijerp:v:13:y:2016:i:10:p:990-:d:79897
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    References listed on IDEAS

    as
    1. Lufen Chang & Michael Karin, 2001. "Mammalian MAP kinase signalling cascades," Nature, Nature, vol. 410(6824), pages 37-40, March.
    2. Fuhong Liu & Bei Wang & Liqun Li & Fengyun Dong & Xiaocui Chen & Yan Li & Xiuzhen Dong & Youichiro Wada & Carolyn M. Kapron & Ju Liu, 2015. "Low-Dose Cadmium Upregulates VEGF Expression in Lung Adenocarcinoma Cells," IJERPH, MDPI, vol. 12(9), pages 1-14, August.
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