Anti-apoptotic effect of phloretin on cisplatin-induced apoptosis in HEI-OC1 auditory cells

Choi, Byung-Min; Chen, Xiao Yan; Gao, Shang Shang; Zhu, Rizhe; Kim, Bok-Ryang

doi:10.1016/s1734-1140(11)70582-5

Cited by 40 publications

(22 citation statements)

References 32 publications

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“…By contrast, Bcl-2 protein disrupts this process and decreases apoptosis (40). It has also been demonstrated that Bcl-2 expression is reduced while that of Bax is increased in HECI-OC1 cells pre-treated with ZnPP (36). Thus, we hypothesized that pre-treatment with ZnPP would promote the release of cytochrome c and the activation of the mitochondrial death cascade.…”

Section: Discussionmentioning

confidence: 94%

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ZnPP reduces autophagy and induces apoptosis, thus aggravating liver ischemia/reperfusion injury in vitro

Wang

Xiong

Guo

et al. 2014

International Journal of Molecular Medicine

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Abstract. There is growing evidence indicating that autophagy plays a protective role in liver ischemia/reperfusion (IR) injury. Heme oxygenase-1 (HO-1) can also prevent liver IR injury by limiting inflammation and inducing an anti-apoptotic response. Autophagy also plays a crucial role in liver IR injury. The aim of the present study was to investigate the role of HO-1 in liver IR injury and the association between HO-1, autophagy and apoptotic pathways. IR simulation was performed using buffalo rat liver (BRL) cells, and HO-1 activity was either induced by hemin (HIR group) or inhibited by zinc protoporphyrin (ZnPP) (ZIR group). In the HIR and ZIR group, the expression of HO-1 and autophagy-related genes [light chain 3-Ⅱ (LC3-Ⅱ)] was assessed by RT-qPCR and the protein expression of caspases, autophagy-related genes and genes associated with apoptotic pathways (Bax) was detected by western blot anlaysis. The results of RT-PCR revealed the genetically decreased expression of HO-1 and autophagy-related genes in the ZIR group. Similar results were obtained by western blot analysis and immunofluorescence. An ultrastructural analysis revealed a lower number of autophagosomes in the ZIR group; in the HIR group, the number of autophagosomes was increased. The expression of Bax and cytosolic cytochrome c was increased, while that of Bcl-2 was decreased following treatment of the cells with ZnPP prior to IR simulation; the oppostie occurred in the HIR group. Cleaved caspase-3, caspase-9 and poly(ADPribose) polymerase (PARP) protein were activated in the IR and ZIR groups. The disruption of mitochondrial membrane potential was also observed in the ZIR group. In general, the downregulation of HO-1 reduced autophagy and activated the mitochondrial apoptotic pathway.

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Section: Discussionmentioning

confidence: 94%

“…However, this was not observed in the control and HIR groups. mechanisms against cisplatin-induced apoptosis (36). Another study found that the induction of HO-1 ameliorated hepatocyte apoptotic activity and oxidative damage in rats with hyperthyroidism, and decreased the expression of cytochrome c, caspase-3, caspase-8 and Bax.…”

Section: Discussionmentioning

confidence: 97%

ZnPP reduces autophagy and induces apoptosis, thus aggravating liver ischemia/reperfusion injury in vitro

Wang

Xiong

Guo

et al. 2014

International Journal of Molecular Medicine

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“…CoPPIX inhibits cisplatin-induced death in the HEI-OC1 auditory-derived cell line (Kim et al 2006a(Kim et al , 2009So et al 2006So et al , 2008Choi et al 2007Choi et al , 2008Choi et al , 2011Gao et al 2010). HO-1 expression has been reported in cochlear hair cells and stria vascularis following a variety of stressors, including noise stress, heat stress, and pharmacological induction (Fairfield et al 2004;Lopez et al 2008;Kim et al 2009;Matsunobu et al 2009;Fetoni et al 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Pharmacological induction of HO-1 is protective against multiple stresses in many tissue types, including ischemia-reperfusion injury in liver and retina (Tsuchihashi et al 2007;Sun et al 2010). Several studies have demonstrated that inducers of HO-1 protect against cisplatin-induced death in the HEI-OC1 auditory cell line (Kim et al 2006a(Kim et al , 2009So et al 2006So et al , 2008Choi et al 2007Choi et al , 2008Choi et al , 2011Gao et al 2010). We have shown that HO-1 induction inhibits hearing loss and hair cell death caused by aminoglycoside antibiotics (Francis et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Heat Shock Protein-Mediated Protection Against Cisplatin-Induced Hair Cell Death

Baker

Roy

Brandon

et al. 2014

JARO

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Cisplatin is a highly successful and widely used chemotherapy for the treatment of various solid malignancies in both adult and pediatric patients. Side effects of cisplatin treatment include nephrotoxicity and ototoxicity. Cisplatin ototoxicity results from damage to and death of cells in the inner ear, including sensory hair cells. We showed previously that heat shock inhibits cisplatin-induced hair cell death in whole-organ cultures of utricles from adult mice. Since heat shock protein 70 (HSP70) is the most upregulated HSP in response to heat shock, we investigated the role of HSP70 as a potential protectant against cisplatin-induced hair cell death. Our data using utricles from HSP70 −/− mice indicate that HSP70 is necessary for the protective effect of heat shock against cisplatin-induced hair cell death. In addition, constitutive expression of inducible HSP70 offered modest protection against cisplatin-induced hair cell death. We also examined a second heat-inducible protein, heme oxygenase-1 (HO-1, also called HSP32). HO-1 is an enzyme responsible for the catabolism of free heme. We previously showed that induction of HO-1 using cobalt protoporphyrin IX (CoPPIX) inhibits aminoglycoside-induced hair cell death. Here, we show that HO-1 also offers significant protection against cisplatin-induced hair cell death. HO-1 induction occurred primarily in resident macrophages, with no detectable expression in hair cells or supporting cells. Depletion of macrophages from utricles abolished the protective effect of HO-1 induction. Together, our data indicate that HSP induction protects against cisplatin-induced hair cell death, and they suggest that resident macrophages mediate the protective effect of HO-1 induction.

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“…Some of the effects are due to estrogenic activity of the substance [13,14,16]. At low concentrations, phloretin has been shown to protect against apoptosis [17]. At high concentrations, phloretin may trigger apoptosis and thus counteract malignancy [1,2,18,19,20,21,22].…”

Section: Introductionmentioning

confidence: 99%

Stimulation of Erythrocyte Death by Phloretin

Bissinger

Fischer

Jilani

et al. 2014

Cell Physiol Biochem

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Background: Phloretin, a natural component of apples, pears and strawberries, has previously been shown to stimulate apoptosis of nucleated cells. Erythrocytes may similarly enter suicidal death or eryptosis, which is characterized by cell shrinkage and phospholipid scrambling of the erythrocyte cell membrane with phosphatidylserine translocation to the erythrocyte surface. Stimulators of eryptosis include increase of cytosolic Ca²⁺-activity ([Ca²⁺]_i), ceramide, ATP depletion, and activation of protein kinase C (PKC) as well as p38 mitogen activated protein kinase (p38 kinase). Methods: Phosphatidylserine exposure at the cell surface was estimated from annexin V binding, cell volume from forward scatter, [Ca²⁺]_i from Fluo3-fluorescence, and ceramide abundance from binding of specific antibodies. Results: A 48 h exposure of human erythrocytes to phloretin significantly increased the percentage of annexin-V-binding cells (≥100 µM) without significantly influencing forward scatter. Phloretin did not significantly modify [Ca²⁺]_i and the stimulation of annexin-V-binding by phloretin (300 µM) did not require presence of extracellular Ca²⁺. Phloretin did not significantly modify erythrocyte ATP levels, and the effect of phloretin on annexin-V-binding was not significantly altered by PKC inhibitor staurosporine (1 µM) or p38 kinase inhibitor SB2203580 (2 µM). However, phloretin significantly increased the ceramide abundance at the cell surface. Conclusions: Phloretin stimulates phospholipid scrambling of the erythrocyte cell membrane, an effect at least partially due to up-regulation of ceramide abundance.

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Anti-apoptotic effect of phloretin on cisplatin-induced apoptosis in HEI-OC1 auditory cells

Cited by 40 publications

References 32 publications

ZnPP reduces autophagy and induces apoptosis, thus aggravating liver ischemia/reperfusion injury in vitro

ZnPP reduces autophagy and induces apoptosis, thus aggravating liver ischemia/reperfusion injury in vitro

Heat Shock Protein-Mediated Protection Against Cisplatin-Induced Hair Cell Death

Stimulation of Erythrocyte Death by Phloretin

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