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[The protein expression profiles induced by trimethyltin chloride in Vero cells]
1Institute of Hygiene, Zhejiang Academy of Medical Sciences, Hangzhou 310013, China.
Objective:
To explore the biomarkers and mechanism of kidney toxicity induced by trimethyltin chloride (TMT-Cl) through analyzing the differences of protein expression profiles between vero cells and vero cells exposed to TMT-Cl.
Methods:
The differences of protein expression levels of three paired samples of vero cells and vero cells exposed to TMT-Cl were compared by two-dimensional gel electrophoresis (2-DE) and liquid chromatography-electrospray ionization-linear trap quadrupole (LC-ESI-LTQ). The differences of expression levels of Annexin A1 and α-Tubulin proteins were validated with western blot assay, and the differences of mRNA expression levels of Annexin A1 and α-Tubulin genes were detected with quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR).
Results:
Fifteen spots of differential expression in protein profiles between vero cells and vero cells exposed to TMT-Cl were found, and 9 of these spots were identified by LC-ESI-LTQ. The expression levels of 3 proteins (Annexin A1,similar to RAN protein and a hypothetical protein) increased and the expression levels of 6 proteins(growth factor receptor-bound protein 10, tubulin alpha 6, heterogeneous nuclear ribonucleoprotein, similar to elongation factor SIII p15 subunit, S-adenosylhomocysteine hydrolase and a hypothetical protein) reduced. The expression levels of α-Tubulin protein and mRNA significantly decreased in vero cells exposed to TMT-Cl, as compared with vero cells (P < 0.01). The expression of Annexin A1 protein in all exposure groups was significantly up-regulated, the expression of Annexin A1 mRNA in the groups exposed to 25 and 50 µmol/L TMT-Cl was significantly down-regulated, and The expression of Annexin A1 mRNA in the group exposed to 100 µmol/L TMT-Cl was significantly up-regulated (P < 0.01).
Conclusions:
The results of present study suggest that 9 proteins with differential expression detected by LC-ESI-LTQ may be related to the kidney toxicity induced by TMT-Cl, which can serve as the biomarkers of early diagnosis and therapeutic effect for the kidney toxicity induced by TMT-Cl.
Insights
Trimethyltin chloride (TMT-Cl) exposure causes kidney toxicity by altering protein expression. Identified proteins like Annexin A1 and α-Tubulin may serve as early biomarkers for TMT-Cl induced kidney toxicity.
Area of Science:
- Proteomics
- Toxicology
- Molecular Biology
Background:
- Trimethyltin chloride (TMT-Cl) is a known nephrotoxicant.
- Understanding the molecular mechanisms of TMT-Cl induced kidney toxicity is crucial for developing diagnostic and therapeutic strategies.
Purpose of the Study:
- To identify potential biomarkers and elucidate the mechanism of kidney toxicity induced by TMT-Cl.
- To analyze differential protein expression profiles in vero cells upon TMT-Cl exposure.
Main Methods:
- Comparative proteomic analysis using two-dimensional gel electrophoresis (2-DE) and liquid chromatography-electrospray ionization-linear trap quadrupole (LC-ESI-LTQ).
- Validation of key protein and mRNA expression levels using western blot and quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR).
Main Results:
- Nine differentially expressed proteins were identified by LC-ESI-LTQ, with 3 showing increased and 6 showing decreased expression.
- Significant down-regulation of α-Tubulin protein and mRNA was observed in TMT-Cl exposed cells.
- Annexin A1 protein was up-regulated, while its mRNA expression showed differential regulation depending on TMT-Cl concentration.
Conclusions:
- The identified 9 differentially expressed proteins are potential biomarkers for early diagnosis and monitoring of TMT-Cl induced kidney toxicity.
- These findings provide insights into the molecular mechanisms underlying TMT-Cl nephrotoxicity.
