ArticleInternational urology and nephrology2016
Proteasome or immunoproteasome inhibitors cause apoptosis in human renal tubular epithelial cells under normoxic and hypoxic conditions.
Article in International urology and nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Renal Implications of Dysregulated Protein Homeostasis: Insights into Ubiquitin-Proteasome and Autophagy Systems.Biomolecules · 2025Review
- On the role of the immunoproteasome in transplant rejection.Immunogenetics · 2019Review
- Immunoproteasome in the blood plasma of children with acute appendicitis, and its correlation with proteasome and UCHL1 measured by SPR imaging biosensors.Clinical and experimental immunology · 2018Article
- Methods for 20S Immunoproteasome and 20S Constitutive Proteasome Determination Based on SPRI Biosensors.Cellular and molecular bioengineering · 2017Article
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5 authors at 1 institution in 1 country.
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Abstract
purposeIschemic acute kidney injury is characterized by apoptosis of tubular epithelial cells. Proteasome plays a key role in cellular processes such as proliferation, apoptosis and inflammation. The results of animal studies about the effect of proteasome inhibitors on the course of ischemic acute kidney injury are controversial.
methodsPrimary human renal tubular epithelial cells were cultured with or without the hypoxia mimetic CoCl2 and with or without the proteasome inhibitor CEP-18770 and/or the immunoproteasome inhibitor ONX-0914. The level of the proteasome subunit β5, the immunoproteasome subunits LMP7 and LMP2, the function of these proteolytic machines, HIF-1α and its transcriptional target lactate dehydrogenase-A, p53 and its transcriptional targets TP53-inducible glycolysis and apoptosis regulator and p21, and finally of activated cleaved caspase-3 were assessed by means of western blotting.
resultsCoCl2 decreased the expression of β5, LMP7 and LMP2, as well as the activity of proteasome and immunoproteasome. It increased HIF-1α and its function, along with p53 and its function and induced apoptosis. CEP-18770 and ONX-0914 induced the above alterations toward the same directions as CoCl2 does. In CoCl2-treated cells, pretreatment with CEP-18770 and/or ONX-0914 potentiates the changes induced by CoCl2 alone.
conclusionCoCl2, CEP-18770 and ONX-0914 induce apoptosis in human renal tubular epithelial cells. Importantly, proteasome or immunoproteasome inhibitors are rather toxic than beneficial in human renal tubular epithelial cells treated with the hypoxia mimetic CoCl2.
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