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Nephrotoxicity Profile of Cadmium Revealed by Proteomics in Mouse Kidney
Xi Sun1, Yanwei Wang1, Tingya Jiang1
1Institute of Life Sciences, Jiangsu University, Zhenjiang, 212013, Jiangsu, China.
Abstract:
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.
Insights
This study reveals how cadmium exposure alters kidney proteins, affecting metabolism and promoting damage. Key proteins involved in cell migration and cancer development were identified, offering insights into cadmium toxicity mechanisms.
Area of Science:
- Toxicology
- Proteomics
- Molecular Biology
Background:
- Cadmium (Cd) is a toxic metal targeting the kidney.
- The molecular mechanisms of Cd-induced kidney damage are not fully understood.
Purpose of the Study:
- To investigate the proteomic changes in the kidney induced by cadmium exposure in a mouse model.
- To identify proteins and pathways affected by cadmium accumulation in the kidney.
Main Methods:
- Two-dimensional gel electrophoresis (2-DE) for protein separation.
- Matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS) for protein identification.
- Gene Ontology (GO) analysis and KEGG pathway annotation.
- Western blotting and RT-qPCR for protein validation.
Main Results:
- 34 differentially expressed proteins were identified in cadmium-exposed mouse kidneys.
- Cadmium exposure altered kidney metabolism, promoted renal damage, and induced cell migration.
- Upregulated proteins included LASP1, PEPCK1, eIF4A, and PNPO; downregulated proteins included ACSM3, PK, and NHERF3.
- Decreased transferrin (TRF) was associated with NHERF3 downregulation and potential renal damage.
Conclusions:
- The study reveals the proteomic profile of cadmium-induced nephrotoxicity.
- Identified protein changes provide insights into the molecular mechanisms of cadmium toxicity and potential links to renal damage and carcinoma development.
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