Hydrogen peroxide induced apoptosis in SV-40 transformed human salivary gland acinar cells

Ben-juan, Wei; Zhou, Zengtong

doi:10.1016/j.oraloncology.2006.03.006

Cited by 5 publications

(2 citation statements)

References 12 publications

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“…The programmed cell death (PCD) of IVD cells plays an important role in this process 7,8 . Apoptosis, a type of programmed cell death in IVDD, is a significant homeostatic mechanism in multicellular organisms, inducing the elimination of senescent cells and seriously damaged cells through an orderly process of cellular disintegration 9 . However, excessive apoptosis leads to a variety of diseases.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial NDUFA4L2 attenuates the apoptosis of nucleus pulposus cells induced by oxidative stress via the inhibition of mitophagy

Zheng

Yang

et al. 2019

Exp Mol Med

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The main pathological mechanism of intervertebral disc degeneration (IVDD) is the programmed apoptosis of nucleus pulposus (NP) cells. Oxidative stress is a significant cause of IVDD. Whether mitophagy is induced by strong oxidative stress in IVDD remains to be determined. This study aimed to investigate the relationship between oxidative stress and mitophagy and to better understand the mechanism of IVDD in vivo and in vitro. To this end, we obtained primary NP cells from the human NP and subsequently exposed them to TBHP. We observed that oxidative stress induced mitophagy to cause apoptosis in NP cells, and we suppressed mitophagy and found that NP cells were protected against apoptosis. Interestingly, TBHP resulted in mitophagy through the inhibition of the HIF-1α/NDUFA4L2 pathway. Therefore, the upregulation of mitochondrial NDUFA4L2 restricted mitophagy induced by oxidative stress. Furthermore, the expression levels of HIF-1α and NDUFA4L2 were decreased in human IVDD. In conclusion, these results demonstrated that the upregulation of NDUFA4L2 ameliorated the apoptosis of NP cells by repressing excessive mitophagy, which ultimately alleviated IVDD. These findings show for the first time that NDUFA4L2 and mitophagy may be potential therapeutic targets for IVDD.

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Section: Introductionmentioning

confidence: 99%

Mitochondrial NDUFA4L2 attenuates the apoptosis of nucleus pulposus cells induced by oxidative stress via the inhibition of mitophagy

Zheng

Yang

et al. 2019

Exp Mol Med

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“…Apoptosis, known as type I PCD, is an essential homeostatic mechanism in multicellular organisms, allowing the elimination of no longer needed or seriously damaged cells by an orderly process of cellular disintegration [3]. It is characterized by caspase activation, cell shrinkage, nuclear and cytoplasmic condensation, DNA fragmentation, and formation of apoptosomes [4].…”

Section: Introductionmentioning

confidence: 99%

The Responses of Autophagy and Apoptosis to Oxidative Stress in Nucleus Pulposus Cells: Implications for Disc Degeneration

Chen

et al. 2014

Cell Physiol Biochem

160

126

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Background/Aims: Apoptosis and autophagy are two patterns of programmed cell death which play important roles in the intervertebral disc degeneration. Oxidative stress is an important factor for the induction of programmed cell death. However, the cellular reactions linking autophagy to apoptosis of disc cells under oxidative stress have never been described. This study investigated the responses of autophagy and apoptosis and their interactions in the nucleus pulposus cells (NP cells) under oxidative stress, with the aim to better understand the mechanism of disc degeneration. Methods: NP cells isolated from rat lumbar discs were subjected to different concentrations of H₂O₂ for various time periods. Cell viability was determined by CCK-8 assay, and their apoptosis and autophagy responses were evaluated by fluorescent analysis, flow cytometry and western blotting, et al. The interactions of autophagy and apoptosis and the possible signaling pathways were also investigated by using autophagy modulators. Results: H₂O₂ increased the lysosomal membrane permeability in the NP cells and induced apoptosis through the mitochondrial pathway subsequently. Meanwhile, H₂O₂ stimulated an early autophagy response through the ERK/m-TOR signaling pathway. Autophagy inhibition significantly decreased the apoptosis incidence in the cells insulted by H₂O₂. Conclusion: These results suggested that controlling the autophagy response in the NP cells under oxidative stress should be beneficial for the survival of the cells and probably delay the process of disc degeneration.

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Apoptotic effects of hydrogen peroxide and vitamin C on chicken embryonic fibroblasts: redox state and programmed cell death

Jin

Yang

et al. 2011

Cytotechnology

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The pro-apoptotic effects of hydrogen peroxide and the purported anti-apoptotic effects of Vitamin C on chicken embryonic fibroblasts were investigated. Hydrogen peroxide induced morphological changes in a dose dependent manner, and a myriad of autophagosomes were observed using transmission electron microscopy. Doxorubicin elicited alterations were not inhibited by co-incubation with Vitamin C except that mitochondrial structure was slightly improved. TUNEL assay, cytotoxicity analysis and flow cytometry revealed that the cytotoxicity, DNA fragmentation and apoptotic rates were dose dependent upon treatment with hydrogen peroxide. Calcium homeostasis was disrupted in a dose dependent manner, and cell cycle was blocked at G(2)/M checkpoint at low concentration and S/G(2) checkpoint at high concentration respectively upon treatment with hydrogen peroxide. The administration of Vitamin C only has a modest effect against doxorubicin induced apoptosis, calcium homeostasis disruption and cell cycle arrest. This research demonstrated that the elevation of reactive oxygen species is sufficient to induce the apoptosis of chicken embryonic fibroblasts, whereas the administration of Vitamin C does not necessarily have certain anti-apoptotic effects, especially when the stimulus is not directly linked with redox state.

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Hydrogen peroxide induced apoptosis in SV-40 transformed human salivary gland acinar cells

Cited by 5 publications

References 12 publications

Mitochondrial NDUFA4L2 attenuates the apoptosis of nucleus pulposus cells induced by oxidative stress via the inhibition of mitophagy

Mitochondrial NDUFA4L2 attenuates the apoptosis of nucleus pulposus cells induced by oxidative stress via the inhibition of mitophagy

The Responses of Autophagy and Apoptosis to Oxidative Stress in Nucleus Pulposus Cells: Implications for Disc Degeneration

Apoptotic effects of hydrogen peroxide and vitamin C on chicken embryonic fibroblasts: redox state and programmed cell death

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