Neuron-derived orphan receptor 1 transduces survival signals in neuronal cells in response to hypoxia-induced apoptotic insults

Chio, Chung-Ching; Li, Wei; Chen, Tyng Guey; Lin, Chien Min; Shieh, Jiunn‐Min; Yeh, Poh‐Shiow; Chen, Ruei Ming

doi:10.3171/2015.6.jns1535

Cited by 18 publications

(26 citation statements)

References 38 publications

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“…In our present study, firstly, the effects of 6G on hypoxia-treated PC-12 cells were measured. In addition, caspases were activated in the process of apoptosis [19]. Autophagy is also a type of cell death which degrades and recycles long-lived or damaged proteins and cytoplasmic organelles by lysosomes [20].…”

Section: Discussionmentioning

confidence: 99%

6-Gingerols (6G) reduces hypoxia-induced PC-12 cells apoptosis and autophagy through regulation of miR-103/BNIP3

Kang

Han

Zhang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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2019) 6-Gingerols (6G) reduces hypoxia-induced PC-12 cells apoptosis and autophagy through regulation of miR-103/BNIP3, Artificial ABSTRACT Finding novel therapeutic agent for the treatment of cerebral ischemia is urgently required. These experiments explored the potential roles of 6-Gingerols (6G) in hypoxia-stimulated rat PC-12 cells. Cell viability, apoptosis and its related proteins were studied by the approaches of MTT assay, flow cytometry assay and Western blot analysis, respectively. In addition, whether 6G achieved its functions in hypoxia-induced injury through miR-103 was illustrated. Moreover, the associated signalling pathways were investigated. Obviously, hypoxia treatment blocked cell viability and enhanced apoptosis while this trend was ameliorated by 6G. Then we observed that hypoxia administration up-regulated miR-103 expression and 6G could further increase miR-103 expression in hypoxia-stimulated PC-12 cells. Inhibition of miR-103 attenuated the neuroprotective effects of 6G on hypoxia-treated PC-12 cells. Moreover, Bcl2/adenovirus EIB 19kD-interacting protein 3 (BNIP3) was a target of miR-103 and BNIP3 upregulation also attenuated the neuroprotective impact of 6G on hypoxia-treated PC-12 cells. Hypoxia activated the p38MAPK and JNK pathways were inactivated by 6G. To sum up, 6G protected hypoxiastimulated PC-12 cells through miR-103-mediatated down-regulation of BNIP3 by inhibiting p38 MAPK and JNK pathways. HIGHLIGHTS 1. 6-Gingerols (6G) is a promising agent for cerebral ischemia therapy. 2. The neuroprotective effects of 6G are mediated by miR-103 and BNIP3. 3. Up-regulation of miR-103 exerts neuroprotective effects. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

6-Gingerols (6G) reduces hypoxia-induced PC-12 cells apoptosis and autophagy through regulation of miR-103/BNIP3

Kang

Han

Zhang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…7B. Interestingly, we identified Nr4a subfamily ( Nr4a1/Nur77 and Nr4a3/Nor1 36, 37 ) which regulates apoptosis and inflammation was significantly decreased in HFD (Fig. 7B).…”

Section: Resultsmentioning

confidence: 80%

Effect of high fat diet on phenotype, brain transcriptome and lipidome in Alzheimer’s model mice

Nam

Mounier

Wolfe

et al. 2017

Sci Rep

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We examined the effect of chronic high fat diet (HFD) on amyloid deposition and cognition of 12-months old APP23 mice, and correlated the phenotype to brain transcriptome and lipidome. HFD significantly increased amyloid plaques and worsened cognitive performance compared to mice on normal diet (ND). RNA-seq results revealed that in HFD mice there was an increased expression of genes related to immune response, such as Trem2 and Tyrobp. We found a significant increase of TREM2 immunoreactivity in the cortex in response to HFD, most pronounced in female mice that correlated to the amyloid pathology. Down-regulated by HFD were genes related to neuron projections and synaptic transmission in agreement to the significantly deteriorated neurite morphology and cognition in these mice. To examine the effect of the diet on the brain lipidome, we performed Shotgun Lipidomics. While there was no difference in the total amounts of phospholipids of each class, we revealed that the levels of 24 lipid sub-species in the brain were significantly modulated by HFD. Network visualization of correlated lipids demonstrated overall imbalance with most prominent effect on cardiolipin molecular sub-species. This integrative approach demonstrates that HFD elicits a complex response at molecular, cellular and system levels in the CNS.

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“…Release of mitochondrial cytochrome c to the cytoplasm can react with apoptotic protease-activating factor-1 (Apaf-1) and apoptosome to form a complex with an assistance of deoxyadenosine triphosphate [Jiang and Wang, 2000]. The multimeric cytochrome c-Apaf-1 complex can then trigger procaspase-9 into its activated form [Jiang and Wang, 2000;Ow et al, 2008;Chio et al, 2016]. In this study, we showed that dexmedetomidine reduced the reperfusion injuryinduced enhancement of caspase-9 protease activity in neuronal cells via suppressing cytochrome c release from mitochondria.…”

Section: Discussionmentioning

confidence: 93%

Protection of Dexmedetomidine Against Ischemia/Reperfusion-Induced Apoptotic Insults to Neuronal Cells Occurs Via an Intrinsic Mitochondria-Dependent Pathway

Tai

Tsai

et al. 2017

J. Cell. Biochem.

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Dexmedetomidine, an agonist of alpha2-adrenergic receptors, is used for critically ill patients to induce and maintain sedation and analgesia. Brain ischemia/reperfusion (I/R) usually causes severe neuronal injuries to intensive care unit patients. This study was aimed to evaluate the effects of dexmedetomidine on I/R-induced insults to neuronal cells and the possible mechanisms. Treatment of neuro-2a cells with dexmedetomidine did not affect cell viability but could protect against I/R-induced cell death. Separately, the I/R-triggered cell shrinkage, DNA fragmentation, and apoptosis in neuro-2a cells were alleviated by dexmedetomidine. As to the mechanisms, exposure of neuro-2a cells to dexmedetomidine substantially attenuated I/R-induced translocation of Bax protein from the cytosol to mitochondria and reduction in the mitochondrial membrane potential (MMP). Successively, dexmedetomidine decreased cytochrome c release from mitochondria to the cytoplasm and consequent cascade activations of caspases-9, -3, and -6 in I/R-treated neuro-2a cells. Interestingly, downregulating caspase-6 activity synergistically improved dexmedetomidine-induced defense against I/R-induced apoptosis of neuro-2a cells. The dexmedetomidine-involved neuroprotection was further confirmed in the other NB41A3 neuronal cells by significantly attenuating I/R-induced changes in the MMP, caspase-3 activation, DNA fragmentation, and cell apoptosis. Taken together, this study has shown the neuroprotective effects of dexmedetomidine against I/R-induced apoptotic insults via an intrinsic Bax-mitochondria-cytochrome c-caspase protease pathway. J. Cell. Biochem. 118: 2635-2644, 2017. © 2016 Wiley Periodicals, Inc.

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Neuron-derived orphan receptor 1 transduces survival signals in neuronal cells in response to hypoxia-induced apoptotic insults

Cited by 18 publications

References 38 publications

6-Gingerols (6G) reduces hypoxia-induced PC-12 cells apoptosis and autophagy through regulation of miR-103/BNIP3

6-Gingerols (6G) reduces hypoxia-induced PC-12 cells apoptosis and autophagy through regulation of miR-103/BNIP3

Effect of high fat diet on phenotype, brain transcriptome and lipidome in Alzheimer’s model mice

Protection of Dexmedetomidine Against Ischemia/Reperfusion-Induced Apoptotic Insults to Neuronal Cells Occurs Via an Intrinsic Mitochondria-Dependent Pathway

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