Next Article in Journal
Deciphering White Adipose Tissue Heterogeneity
Previous Article in Journal
Transcriptome Analysis of Yamame (Oncorhynchus masou) in Normal Conditions after Heat Stress
Article Menu
Issue 2 (June) cover image

Export Article

Open AccessArticle

Factors that May Protect the Native Hibernator Syrian Hamster Renal Tubular Epithelial Cells from Ferroptosis Due to Warm Anoxia-Reoxygenation

Department of Nephrology, Faculty of Medicine, University of Thessaly, 41110 Larissa, Greece
Author to whom correspondence should be addressed.
Biology 2019, 8(2), 22;
Received: 27 January 2019 / Revised: 26 March 2019 / Accepted: 27 March 2019 / Published: 31 March 2019
PDF [1877 KB, uploaded 31 March 2019]
  |     |  


Warm anoxia-reoxygenation induces ferroptotic cell death in mouse proximal renal tubular epithelial cells (RPTECs), whereas RPTECs of the native hibernator Syrian hamster resist cell death. Clarifying how hamster cells escape ferroptosis may reveal new molecular targets for preventing or ameliorating ischemia-reperfusion-induced human diseases or expanding the survival of organ transplants. Mouse or hamster RPTECs were subjected to anoxia and subsequent reoxygenation. Cell death was assessed with the lactated dehydrogenase (LDH) release assay and lipid peroxidation by measuring cellular malondialdehyde (MDA) fluorometrically. The effect of the ferroptosis inhibitor α-tocopherol on cell survival was assessed by the 2,3-bis (2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino) carbonyl]-2H-tetrazolium hydroxide (XTT) assay. The expression of the critical ferroptotic elements cystine-glutamate antiporter (xCT), ferritin, and glutathione peroxidase 4 (GPX4) was assessed by Western blot. Contrary to mouse RPTECs, hamster RPTECs resisted anoxia-reoxygenation-induced cell death and lipid peroxidation. In mouse RPTECs, α-tocopherol increased cell survival. Anoxia increased the levels of xCT, ferritin, and GPX4 in both cell types. During reoxygenation, at which reactive oxygen species overproduction occurs, xCT and ferritin decreased, whereas GPX4 increased in mouse RPTECs. In hamster RPTECs, reoxygenation raised xCT and ferritin, but lowered GPX4. Hamster RPTECs resist lipid peroxidation-induced cell death. From the three main evaluated components of the ferroptotic pathway, the increased expression of xCT and ferritin may contribute to the resistance of the hamster RPTECs to warm anoxia-reoxygenation. View Full-Text
Keywords: hibernation; ischemia-reperfusion; ferroptosis; xCT; ferritin; GPX4 hibernation; ischemia-reperfusion; ferroptosis; xCT; ferritin; GPX4

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Eleftheriadis, T.; Pissas, G.; Liakopoulos, V.; Stefanidis, I. Factors that May Protect the Native Hibernator Syrian Hamster Renal Tubular Epithelial Cells from Ferroptosis Due to Warm Anoxia-Reoxygenation. Biology 2019, 8, 22.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Biology EISSN 2079-7737 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top