Decreased Poly(ADP-Ribose) Polymerase 1 Expression Attenuates Glucose Oxidase-Induced Damage in Rat Cochlear Marginal Strial Cells

Zhang, Yuanyuan; Yang, Yang; Xie, Zhen; Zuo, Wenqi; Jiang, Hongyan; Zhao, Xueyan; Sun, Yu; Kong, Weijia

doi:10.1007/s12035-015-9469-7

Cited by 14 publications

(12 citation statements)

References 47 publications

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“…Some evidence revealed that pro‐caspase 3 was the precursor of the caspase‐3. Caspase‐3 was activated by cleaving pro‐caspase 3, while activated caspase‐3 further cleaved PARP‐1 resulting in cell apoptosis . Although it is not known why pro‐caspase 3 expression is higher in TK6‐shPARP‐1 cells, it may contribute to PARP defects.…”

Section: Discussionmentioning

confidence: 99%

Hydroquinone induces TK6 cell growth arrest and apoptosis through PARP‐1/p53 regulatory pathway

Luo

Liang

Chen

et al. 2017

Environmental Toxicology

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Hydroquinone (HQ), one of the most important metabolites derived from benzene, induces cell cycle arrest and apoptosis. Poly(ADP-ribose) polymerase-1 (PARP-1) participates in various biological processes, including DNA repair and cell cycle regulation. To explore whether PARP-1 regulatory pathway mediated HQ-induced cell cycle arrest and apoptosis, we assessed the effect of PARP-1 suppression on induction of apoptosis analyzed by FACSCalibur flow cytometer in PARP-1 deficientTK6 cells (TK6-shPARP-1). We observed an increase in the fraction of cells in G1 phase by 7.6% and increased apoptosis by 4.5% in PARP-1-deficient TK6 cells (TK6-shPARP-1) compared to those negative control cells (TK6-shNC cells) in response to HQ treatment. Furthermore, HQ might activate the extrinsic pathways of apoptosis via up-regulation of Fas expression, followed by caspase-3 activation, apoptotic body, and sub G1 accumulation. Enhanced p53 expression was observed in TK6-shPARP-1 cells than in TK6-shNC cells after HQ treatment. In contrast, Fas expression was lower in TK6-shPARP-1 cells than in TK6-shNC cells. Therefore, we conclude that HQ may activate apoptotic signals via Fas up-regulation and p53-mediated apoptosis in TK6-shNC cells. The reduction of PARP-1 expression further intensified up-regulation of p53 in TK6-shPARP-1 cells, resulting in an increased G1→S phase cell arrest and apoptosis in TK6-shPARP-1 cells compared to TK6-shNC cells.

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Section: Discussionmentioning

confidence: 99%

Hydroquinone induces TK6 cell growth arrest and apoptosis through PARP‐1/p53 regulatory pathway

Luo

Liang

Chen

et al. 2017

Environmental Toxicology

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“…Then the samples were centrifuged for 5 min at 800 g and plated in Epithelial Cell Medium-animal (EpiCM-animal, ScienCell, USA) at 37 °C in a humidified incubator with 5% CO2. The identification of primary MCs by cytokeratin-18, a characteristic molecule of MCs [35] , [36] , was performed as described previously [37] .…”

Section: Methodsmentioning

confidence: 99%

“…The recombinant adenoviruses for interference vector of PARP-1 (Ad-PARP-1-RNAi) and control vector (Ad-Con) were purchased from GeneChem (Shanghai, China). MCs transfection was performed as described previously [37] . A multiplicity of infection (MOI; 30) for Ad-Con and Ad-PARP-1-RNAi was used.…”

Section: Methodsmentioning

confidence: 99%

The dual role of poly(ADP-ribose) polymerase-1 in modulating parthanatos and autophagy under oxidative stress in rat cochlear marginal cells of the stria vascularis

et al. 2018

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Oxidative stress is reported to regulate several apoptotic and necrotic cell death pathways in auditory tissues. Poly(ADP-ribose) polymerase-1 (PARP-1) can be activated under oxidative stress, which is the hallmark of parthanatos. Autophagy, which serves either a pro-survival or pro-death function, can also be stimulated by oxidative stress, but the role of autophagy and its relationship with parthanatos underlying this activation in the inner ear remains unknown. In this study, we established an oxidative stress model in vitro by glucose oxidase/glucose (GO/G), which could continuously generate low concentrations of H2O2 to mimic continuous exposure to H2O2 in physiological conditions, for investigation of oxidative stress-induced cell death mechanisms and the regulatory role of PARP-1 in this process. We observed that GO/G induced stria marginal cells (MCs) death via upregulation of PARP-1 expression, accumulation of polyADP-ribose (PAR) polymers, decline of mitochondrial membrane potential (MMP) and nuclear translocation of apoptosis-inducing factor (AIF), which all are biochemical features of parthanatos. PARP-1 knockdown rescued GO/G-induced MCs death, as well as abrogated downstream molecular events of PARP-1 activation. In addition, we demonstrated that GO/G stimulated autophagy and PARP-1 knockdown suppressed GO/G-induced autophagy in MCs. Interestingly, autophagy suppression by 3-Methyladenine (3-MA) accelerated GO/G-induced parthanatos, indicating a pro-survival function of autophagy in GO/G-induced MCs death. Taken together, these data suggested that PARP-1 played dual roles by modulating parthanatos and autophagy in oxidative stress-induced MCs death, which may be considered as a promising therapeutic target for ameliorating oxidative stress-related hearing disorders.

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“…Results here suggest that that PARP‐1 facilitates cochlear hair cells DNA repair and help maintain genomic stability when DNA damage is slight. However, excessive DNA damage can cause overactivation of PARP‐1 and cell death (Smith, Groves, & Coffin, ; Zhang et al, ). It is speculated that baicalin can work as a PARP‐1 inhibitor to inhibit PARP‐1 overactivation.…”

Section: Discussionmentioning

confidence: 99%

Baicalin attenuates gentamicin‐induced cochlear hair cell ototoxicity

Xian-fen

2019

J of Applied Toxicology

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Gentamicin can lead to cochlear hair cells associated ototoxicity by inducing apoptosis and oxidative stress, which can be alleviated by baicalin, one flavonoid extracted from the root of Scutellaria baicalensis. The role of baicalin in protecting gentamicin-induced hearing loss is unclear. Interference with oxidative stress was investigated in this study using House Ear Institute-Organ of Corti1 (HEI-OC1) cells, which were simultaneously treated with baicalin (0-400 μM) and gentamicin (0.2 or 1 mM). MTT was used to assay cell viability and apoptosis was detected with Annexin V-fluorescein isothiocyanate staining. The production of reactive oxygen species was indicated by 2,7-dichlorofluorescein diacetate fluorescence intensity and mitochondrial depolarization was assayed by JC1-mitochondrial membrane potential assay. Poly(ADP-ribose) polymerase (PARP), cleaved-caspase 3 and cleaved-PARP expression were analyzed with western blot. Baicalin improved the viability of HEI-OC1 cells and significantly reduced the oxidative stress and mitochondrial depolarization compared with the gentamicin treatment group. Gentamicin treatment increased the activation of PARP and caspase-3, while such an increase could be downregulated by baicalin. Baicalin attenuates gentamicin-induced cochlear hair cells ototoxicity, and such inhibition may be mediated by the regulation of reactive oxygen species production, mitochondrial depolarization, and caspase-3 and PARP activation.

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Decreased Poly(ADP-Ribose) Polymerase 1 Expression Attenuates Glucose Oxidase-Induced Damage in Rat Cochlear Marginal Strial Cells

Cited by 14 publications

References 47 publications

Hydroquinone induces TK6 cell growth arrest and apoptosis through PARP‐1/p53 regulatory pathway

Hydroquinone induces TK6 cell growth arrest and apoptosis through PARP‐1/p53 regulatory pathway

The dual role of poly(ADP-ribose) polymerase-1 in modulating parthanatos and autophagy under oxidative stress in rat cochlear marginal cells of the stria vascularis

Baicalin attenuates gentamicin‐induced cochlear hair cell ototoxicity

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