Gene networking in colistin-induced nephrotoxicity reveals an adverse outcome pathway triggered by proteotoxic stress

Colistin has been widely used for the treatment of infections of multidrug-resistant Gram-negative bacteria, despite the fact that it induces serious kidney injury as a side effect. To investigate the mechanism underlying its nephrotoxicity, colistin methanesulfonate sodium (CMS; 25 or 50 mg/kg) was...

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Bibliographic Details
Published in:International journal of molecular medicine 2019-03, Vol.43 (3), p.1343-1355
Main Authors: Lee, Eun Hee, Kim, Soojin, Choi, Mi-Sun, Yang, Heeyoung, Park, Se-Myo, Oh, Hyun-A, Moon, Kyoung-Sik, Han, Ji-Seok, Kim, Yong-Bum, Yoon, Seokjoo, Oh, Jung-Hwa
Format: Article
Language:English
Subjects:
Antibacterial agents
Bacteria
Biochemistry
Care and treatment
Cell cycle
Cell death
Colistin
Complications and side effects
Gene expression
Genes
Genetic aspects
Genomes
Genomics
Genotypes
Gram-negative bacteria
Gram-negative bacterial infections
Health aspects
Heat shock proteins
Histochemistry
Infection
Kidney diseases
Kidneys
Kinases
Microbial drug resistance
Nitric oxide
Oxidative stress
Protein folding
Risk factors
Rodents
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Summary:Colistin has been widely used for the treatment of infections of multidrug-resistant Gram-negative bacteria, despite the fact that it induces serious kidney injury as a side effect. To investigate the mechanism underlying its nephrotoxicity, colistin methanesulfonate sodium (CMS; 25 or 50 mg/kg) was administered via intraperitoneal injection to Sprague-Dawley rats daily over 7 days. Serum biochemistry and histopathology indicated that nephrotoxicity occurred in the rats administered with CMS. Whole-genome microarrays indicated 894 differentially expressed genes in the group treated with CMS (analysis of variance, false discovery rate
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2019.4052