In vitro evaluation of biomarkers of nephrotoxicity through gene expression using gentamicin.
Maria A A CamposLeonardo Augusto de AlmeidaMarina F GrossiCarlos A TagliatiPublished in: Journal of biochemical and molecular toxicology (2018)
Acute renal failure is one of the most frequent effects observed after taking medicine. Such situations have been tardily discovered, given that existing methods for assessing toxicity are not predictive. In this light, the present work evaluated the effects of gentamicin, a form of nephrotoxic drug, on HK-2 and HEK-293 cells. By using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and flow cytometry, both cells demonstrated that cytotoxicity occurs in a dose-dependent manner through the processes of apoptosis and cell necrosis. Gene expression analysis showed a relative increase of expression for genes related to cell processes and classic biomarkers, such as TP53, CASP3, CASP8, CASP9, ICAM-1, EXOC3, KIM-1, and CST3. A decrease in expression for genes BCL2L1 and EGF was observed. This study, therefore, indicates that, when the methods are used together, gene expression analysis is able to evaluate the nephrotoxic potential of a substance.
Keyphrases
- genome wide identification
- cell cycle arrest
- induced apoptosis
- genome wide
- gene expression
- flow cytometry
- poor prognosis
- transcription factor
- oxidative stress
- cell death
- endoplasmic reticulum stress
- single cell
- drug induced
- cell therapy
- dna methylation
- pi k akt
- copy number
- liver failure
- genome wide analysis
- signaling pathway
- stem cells
- intensive care unit
- respiratory failure
- bioinformatics analysis
- endothelial cells
- high glucose