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Chronic cadmium exposure induces transcriptional activation of the Wnt pathway and upregulation of epithelial-to-mesenchymal transition markers in mouse kidney.

Abstract：

:The transition metal cadmium (Cd) is an environmental pollutant which damages the kidneys. Chronic Cd exposure may induce renal fibrosis and/or cancer, but the signaling pathways involved are not understood. The Wnt pathway is a key signaling cascade responsible for renal development, fibrosis and cancer. Hence the effect of chronic in vivo Cd exposure (100 mg/l drinking water for 12 weeks) on transcriptional activation of the Wnt pathway and markers of epithelial-to-mesenchymal transition (EMT) was investigated in mouse kidneys. Cd exposure increased kidney Cd content from 0.023+/-0.001 microg/g to 61+/-7 microg/g wet weight (means+/-S.D. of 6-7 animals). This was accompanied by increased expression of Wnt ligands (Wnt3a/6/7a/7b/9a/9b/10a/11), as determined by RT-PCR. The Wnt receptors Frizzled (Fz1/2/4,5,7-10) were also upregulated, as were the co-receptors low-density lipoprotein receptor-related proteins 5/6. Immunoblots with Wnt10a and Fz7 antibodies also revealed increased protein expression induced by Cd exposure. In contrast, Wnt antagonists were largely unaffected. Upregulation of Wnt signaling components induced by Cd was corroborated by increased expression of Wnt target genes, i.e. cell proliferation and survival genes c-Myc, cyclin D1 and the multidrug transporter P-glycoprotein Abcb1b, which promote malignancy. Lastly the EMT markers Twist, fibronectin and collagen I, but not alpha-smooth muscle actin, were also upregulated, suggesting that Cd-induced changes of renal epithelial tissue characteristics towards fibrosis and cancer may be mediated by Wnt signaling.

journal_name

Toxicol Lett

journal_title

Toxicology letters

authors

Chakraborty PK,Scharner B,Jurasovic J,Messner B,Bernhard D,Thévenod F

doi

10.1016/j.toxlet.2010.05.007

subject

Has Abstract

pub_date

2010-09-15 00:00:00

pages

69-76

issue

1

eissn

0378-4274

issn

1879-3169

pii

S0378-4274(10)01510-9

journal_volume

198

pub_type

杂志文章

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