ArticleIranian journal of basic medical sciences2018
Hypoxia-reoxygenation induced necroptosis in cultured rat renal tubular epithelial cell line.
Article in Iranian journal of basic medical sciences, 2018. 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, 4 citations in OpenAlex.
- Mechanisms and therapeutic prospects of hypoxia-inducible factor 1-alpha in acute kidney injury: a systematic review.Frontiers in cell and developmental biology · 2025Review
- Soluble receptor for advanced glycation end products protects from ischemia- and reperfusion-induced acute kidney injury.Biology open · 2022Article
- Activation of Delta-Opioid Receptor Protects ARPE19 Cells against Oxygen-Glucose Deprivation/Reoxygenation-Induced Necroptosis and Apoptosis by Inhibiting the Release of TNF-Journal of ophthalmology · 2022Article
- Sirtuin 3 deficiency exacerbates diabetic cardiomyopathy via necroptosis enhancement and NLRP3 activation.Acta pharmacologica Sinica · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe aim of this study is to explore the potential role of hypoxia/reoxygenation in necroptosis in cultured rat renal tubular epithelial cell line NRK-52E, and further to investigate its possible mechanisms. MATERIALS AND
methodsCells were cultured under different hypoxia-reoxygenation conditions
resultsMTT assay indicated that hypoxia-reoxygenation treatment can cause a decrease in cell viability. Particularly, 6 hr of hypoxia and 24 hr of reoxygenation (H6R24 group) resulted in the lowest cell viability. Western-blot results indicated that the expression of RIP3 significantly increased in H6R24 group while the expression of NF-κB is decreased. Co-IP results demonstrated that the interaction between RIP1 and RIP3 was stronger in the hypoxia-reoxygenation induced group than the other groups, furthermore, treatment with Nec-1 reduced the formation of necrosome. TEM observation results showed that hypoxia-reoxygenation treated cells showed typical morphological characteristics of necroptosis and autophagy.
conclusionHypoxia-reoxygenation treatment can induce necroptosis in NRK-52E cells, and this effect can be inhibited by Nec-1. In addition, the mechanism of necroptosis induced by hypoxia-reoxygenation injury on cells may be related to the low expression of NF-κB.
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