Neutrophil gelatinase-associated lipocalin production negatively correlates with HK-2 cell impairment: Evaluation of NGAL as a marker of toxicity in HK-2 cells
Language English Country Great Britain, England Media print-electronic
Document type Journal Article
PubMed
27888128
DOI
10.1016/j.tiv.2016.11.012
PII: S0887-2333(16)30243-0
Knihovny.cz E-resources
- Keywords
- Cell viability, HK-2 cells, In vitro nephrotoxicity, NGAL, Nephrotoxicity markers,
- MeSH
- Acute Kidney Injury chemically induced metabolism MeSH
- Biomarkers metabolism MeSH
- Cell Line MeSH
- Cisplatin toxicity MeSH
- Gentamicins toxicity MeSH
- Cadmium toxicity MeSH
- Humans MeSH
- Lipocalin-2 genetics metabolism MeSH
- Acetaminophen toxicity MeSH
- Mercury toxicity MeSH
- tert-Butylhydroperoxide toxicity MeSH
- Cell Survival drug effects MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Biomarkers MeSH
- Cisplatin MeSH
- Gentamicins MeSH
- Cadmium MeSH
- LCN2 protein, human MeSH Browser
- Lipocalin-2 MeSH
- Acetaminophen MeSH
- Mercury MeSH
- tert-Butylhydroperoxide MeSH
Neutrophil gelatinase-associated lipocalin is an extracellular protein produced mostly in kidney. Recently, it has become a promising biomarker of renal damage in vivo. On the other hand, the validation of NGAL as a biomarker for nephrotoxicity estimation in vitro has not been characterized in detail yet. Since the HK-2 cells are frequently used human kidney cell line, we aimed to characterize the production of NGAL in these cells and to evaluate NGAL as a possible marker of cell impairment. We used heavy metals (mercury, cadmium), peroxide, drugs (acetaminophen, gentamicin) and cisplatin to mimic nephrotoxicity. HK-2 cells were incubated with selected compounds for 1-24h and cell viability was measured together with extracellular NGAL production. We proved that HK-2 cells possess a capacity to produce NGAL in amount of 2pg/ml/h. We found a change in cell viability after 24h incubation with all tested toxic compounds. The largest decrease of the viability was detected in mercury, acetaminophen, cisplatin and gentamicin. Unexpectedly, we found also a significant decrease in NGAL production in HK-2 cells treated with these toxins for 24h: to 11±5%, 54±5%, 57±6% and 76±9% respectively, compared with controls (=100%). Our results were followed with qPCR analysis when we found no significant increase in LCN2 gene expression after 24h incubation. We conclude that extracellular NGAL production negatively correlates with HK-2 cell impairment.
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