期刊
BIOLOGICAL TRACE ELEMENT RESEARCH
卷 199, 期 5, 页码 1929-1940出版社
SPRINGERNATURE
DOI: 10.1007/s12011-020-02312-7
关键词
Cadmium; Nephrotoxicity; Proteomics; Metabolism; Migration
资金
- National Natural Science Foundation of China [31600952, 31271272]
- Start-Up Research Funding of Jiangsu University for Distinguished Scholars [5501330001]
This study investigated the proteomic profile changes induced by cadmium in the kidney using a mouse model. It was found that cadmium regulates kidney metabolism, promotes renal damage and cell migration. The downregulation of Na(+)/H(+) exchange regulatory cofactor (NHERF3) could contribute to renal damage, along with a decrease in transferrin (TRF) in the kidney.
Cadmium (Cd) is a highly toxic metal and kidney is its main target. However, the molecular effects and associated potential impacts of Cd-accumulated kidney have not been well investigated. In this study, mouse was used as a model to investigate the Cd-induced proteomic profile change in kidney, and a total of 34 differentially expressed proteins were detected by two-dimensional gel electrophoresis (2-DE) and further identified by matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS). Through Gene Ontology analysis and KEGG pathway annotation, it showed that Cd-regulated kidney metabolism and promoted renal damage and cell migration. By validation of Western blotting and RT-qPCR, metastasis-related proteins LIM and SH3 domain protein 1 (LASP1) and phosphoenolpyruvate carboxykinase/cytosolic [GTP] (PEPCK1) were confirmed to be upregulated; Acyl-CoA synthetase medium-chain family member 3 (ACSM3) was downregulated. Furthermore, carcinoma development-related proteins initiation factor 4A (eIF4A) and pyridoxine-5 '-phosphate oxidase (PNPO) were upregulated, and pyridoxal kinase (PK) was downregulated. The downregulation of Na(+)/H(+) exchange regulatory cofactor (NHERF3) might promote renal damage which associated with decrease of transferrin (TRF) in kidney. Taken together, our results revealed proteomic profile of Cd-induced nephrotoxicity and provided data for further insights into the mechanisms of Cd toxicity.
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