ArticleMolecular medicine reports2017
Altered gene expression profile in a rat model of gentamicin-induced ototoxicity and nephrotoxicity, and the potential role of upregulated Ifi44 expression.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 17 citations in OpenAlex.
- Modulating platelet-activating factor by rupatadine attenuates gentamicin-induced nephrotoxicity in rats via NF-κB/caspase-3 and Nrf2/HO-1 signaling cascades.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The potential role of upregulated PARP-1/RIPK1 expressions in amikacin-induced oxidative damage and nephrotoxicity in Wistar rats.Toxicology research · 2023Article
- Comparison of chondrogenesis-related biological behaviors between human urine-derived stem cells and human bone marrow mesenchymal stem cells from the same individual.Stem cell research & therapy · 2021Article
- Identification of pathogenic genes and transcription factors in respiratory syncytial virus.BMC pediatrics · 2021Article
- Article
- Pioglitazone Ameliorates Gentamicin Ototoxicity by Affecting the TLR and STAT Pathways in the Early Postnatal Organ of Corti.Frontiers in cellular neuroscience · 2020Article
- Irbesartan Attenuates Gentamicin-induced Nephrotoxicity in Rats through Modulation of Oxidative Stress and Endogenous Antioxidant Capacity.International journal of preventive medicine · 2020Article
- Gene expression profiles of germ-free and conventional piglets from the same litter.Scientific reports · 2018Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As demonstrated by Alport syndrome, the co‑occurrence of auditory and urinary system malformations, and gentamicin-induced ototoxicity and nephrotoxicity, the ears and kidneys potentially share certain molecular pathways. In the present study, microarray chips were used to analyze the changes in the gene expression profile using a rat model of gentamicin‑induced ototoxicity and nephrotoxicity, using rat liver tissue as a control. A number of genes were identified to exhibit similar expression changes in the rat ears and kidney tissues, among which microtubule‑associated protein 44 (Ifi44), was selected for further analysis to validate its expression changes and confirm potential involvement in the inflammation process in the disease model. Ifi44 is a member of the type I interferon‑inducible gene family. Reverse transcription‑quantitative polymerase chain reaction, western blotting and immunohistochemistry were performed; the results demonstrated that more inflammatory cells were present in cochlear and renal parenchyma in gentamycin‑induced rats, and Ifi44 expression was increased in these two organs compared with control rats. Taken together, with its role in lupus nephritis and expression in the inner ear, the results suggested that Ifi44 is potentially involved in the inflammation associated with gentamicin‑induced ototoxicity and nephrotoxicity. The approach of the current study has also provided a strategy for delineating common pathways shared by organs involved in specific diseases.
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