Energy handling in renal tubular epithelial cells of the hamster, a native hibernator, under warm anoxia or reoxygenation

Eleftheriadis, Theodoros; Pissas, Georgios; Antoniadi, Georgia; Golfinopoulos, Spyridon; Liakopoulos, Vassilios; Stefanidis, Ioannis

doi:10.3892/br.2018.1157

Cited by 4 publications

(3 citation statements)

References 28 publications

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“…Interestingly, the peIF2α-ATF4 axis upregulates xCT [35], and in an experimental model similar to the present study, increased peIF2α levels were observed under anoxia in both mouse and hamster RPTECs [25]. However, in that study, in hamster RPTECs, reoxygenation significantly decreased peIF2α below the control levels, while xCT expression was significantly elevated.…”

Section: Discussionsupporting

confidence: 72%

“…Interestingly, these GPX4 alterations in both mouse and hamster RPTECs followed the same fluctuations as observed in similar experimental conditions regarding the level of the endoplasmic reticulum (ER) stress sensor phosphorylated protein kinase RNA-like ER kinase (pPERK) [24], and of the phosphorylated eukaryotic translation initiation factor 2α (peIF2α) [25]. Thus, it is possible that the observed GPX4 alterations in mouse and hamster RPTECs under anoxia or reoxygenation of the present study may result from corresponding changes of the pPERK-peIF2α-activating transcription factor 4 (ATF4)-heatshock 70-kDa protein 5 (HSPA5) axis since HSPA5 binds to GPX4 and protects it from degradation [26].…”

Section: Discussionmentioning

confidence: 87%

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

Eleftheriadis

Pissas

Liakopoulos

et al. 2019

Biology

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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.

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Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 87%

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

Eleftheriadis

Pissas

Liakopoulos

et al. 2019

Biology

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“…However, as already noted, our study could be considered as a starting point for further investigation of the mechanisms that offer resistance to I-R injury in hibernators. For instance, recently, our team revealed significant differences in energy handling between RPTECs derived from the native hibernator Syrian hamster and the non-hibernator mouse [47]. Also, sometimes ex vivo experiments are required for clarifying the exact molecular mechanisms and the sequence of the events that lead to a certain end-point.…”

Section: Discussionmentioning

confidence: 99%

Cell Death Patterns Due to Warm Ischemia or Reperfusion in Renal Tubular Epithelial Cells Originating from Human, Mouse, or the Native Hibernator Hamster

Eleftheriadis

Pissas

Antoniadi

et al. 2018

Biology

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Ischemia–reperfusion injury contributes to the pathogenesis of many diseases, with acute kidney injury included. Hibernating mammals survive prolonged bouts of deep torpor with a dramatic drop in blood pressure, heart, and breathing rates, interspersed with short periods of arousal and, consequently, ischemia–reperfusion injury. Clarifying the differences under warm anoxia or reoxygenation between human cells and cells from a native hibernator may reveal interventions for rendering human cells resistant to ischemia–reperfusion injury. Human and hamster renal proximal tubular epithelial cells (RPTECs) were cultured under warm anoxia or reoxygenation. Mouse RPTECs were used as a phylogenetic control for hamster cells. Cell death was assessed by both cell imaging and lactate dehydrogenase (LDH) release assay, apoptosis by cleaved caspase-3, autophagy by microtubule-associated protein 1-light chain 3 B II (LC3B-II) to LC3B-I ratio, necroptosis by phosphorylated mixed-lineage kinase domain-like pseudokinase, reactive oxygen species (ROS) fluorometrically, and lipid peroxidation, the end-point of ferroptosis, by malondialdehyde. Human cells died after short periods of warm anoxia or reoxygenation, whereas hamster cells were extremely resistant. In human cells, apoptosis contributed to cell death under both anoxia and reoxygenation. Although under reoxygenation, ROS increased in both human and hamster RPTECs, lipid peroxidation-induced cell death was detected only in human cells. Autophagy was observed only in human cells under both conditions. Necroptosis was not detected in any of the evaluated cells. Clarifying the ways that are responsible for hamster RPTECs escaping from apoptosis and lipid peroxidation-induced cell death may reveal interventions for preventing ischemia–reperfusion-induced acute kidney injury in humans.

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Anti-Apoptotic Effect of Synthetic Leu-Enkephalin Dalargin on Rat Leukocytes in Cold Stress Model in Vivo

Shcheniavsky

2021

Probl Cryobiol Cryomed

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In this research, a protective effect of synthetic analogue of leu-enkephalin dalargin on peripheral blood leukocytes of cold stress-exposed homeotherms has been investigated. The impact of this peptide and in vivo cold stress on cell composition of leukoconcentrate, leukocyte viability and DNA fragmentation degree in rat leukocytes, has been studied by using confocal microscopy. A decreased relative count of lymphocytes and an increased neutrophil one were established as significantly less pronounced in the animals injected with dalargin before cooling, than in non-handled ones. The dalargin administration was also shown to enhance the viability of peripheral blood leukocytes in rats exposed to cold stress. Preliminary administration of dalargin to animals significantly reduced both the degree of DNA fragmentation and a relative count of leukocytes with fragmented DNA in peripheral blood. Simultaneous introduction of opioid receptor antagonist naloxone to animals eliminated a protective effect of opioid receptor agonist dalargin. Our findings demonstrated the opioid receptor-mediated antiapoptotic effect of dalargin on peripheral blood leukocytes under in vivo cold stress.

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Energy handling in renal tubular epithelial cells of the hamster, a native hibernator, under warm anoxia or reoxygenation

Cited by 4 publications

References 28 publications

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

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

Cell Death Patterns Due to Warm Ischemia or Reperfusion in Renal Tubular Epithelial Cells Originating from Human, Mouse, or the Native Hibernator Hamster

Anti-Apoptotic Effect of Synthetic Leu-Enkephalin Dalargin on Rat Leukocytes in Cold Stress Model in Vivo

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