Appoptosin Mediates Lesions Induced by Oxidative Stress Through the JNK-FoxO1 Pathway

Zhang, Cuilin; Tan, Zhenqiu; Xie, Yongzhuang; Zhao, Yingjun; Huang, Timothy; Lu, Z C; Luo, Hong; Can, Dan; Xu, Huaxi; Zhang, Yunwu; Zhang, Xian

doi:10.3389/fnagi.2019.00243

Cited by 9 publications

(5 citation statements)

References 59 publications

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“…Oxidative stress is a major trigger of follicular atresia and GC apoptosis which impairs follicular development, leads to a variety of ovarian diseases, and limits the fertility of female animals including pigs [ 49 , 50 , 51 ]. FoxO1 is a major sensor and effector of oxidative stress [ 52 ] which can promote cell apoptosis in response to oxidative stress by activating downstream apoptosis-related proteins such as Bim [ 53 ], P21 [ 54 ], and Fasl [ 55 ]. Similarly, it has also been reported that inhibiting FoxO1 by different means can effectively block the effect of oxidative stress [ 56 ].…”

Section: Discussionmentioning

confidence: 99%

A Mutation in Endogenous saRNA miR-23a Influences Granulosa Cells Response to Oxidative Stress

Wang

Zeng

et al. 2022

Antioxidants

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Phenotypes are the result of the interaction between the gene and the environment, so the response of individuals with different genotypes to an environment is variable. Here, we reported that a mutation in miR-23a influences granulosa cells (GCs) response to oxidative stress, a common mechanism of environmental factors affecting female reproduction. We showed that nuclear miR-23a is a pro-apoptotic miRNA in porcine GCs through the activation of the transcription and function of NORHA, a long non-coding RNA (lncRNA) induces GC apoptosis and responses to oxidative stress. Mechanistically, miR-23a acts as an endogenous small activating RNA (saRNA) to alter histone modifications of the NORHA promoter through the direct binding to its core promoter. A C > T mutation was identified at −398 nt of the miR-23a core promoter, which created a novel binding site for the transcription factor SMAD4 and recruited the transcription repressor SMAD4 to inhibit miR-23a transcription and function in GCs. Notably, g.−398C > T mutation in the miR-23a promoter reduced GCs response to oxidative stress. In addition, g.−398C > T mutation was significantly associated with sow fertility traits. In short, our findings preliminarily revealed the genetic basis of individual differences in the response to oxidative stress from the perspective of a single mutation and identified miR-23a as a candidate gene for the environmental adaptation to oxidative stress.

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Section: Discussionmentioning

confidence: 99%

A Mutation in Endogenous saRNA miR-23a Influences Granulosa Cells Response to Oxidative Stress

Wang

Zeng

et al. 2022

Antioxidants

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“…The c-Jun N-terminal kinase (JNK) signaling cascade is triggered in response to a broad spectrum of stressors 49 . Of particular relevance to AD, JNK-MAPK proteins are involved in the regulation of apoptosis during oxidative damage through phosphorylation of effector proteins or transcription factors, which may lead to dysregulation of tau phosphorylation and accumulation of hyperphosphorylated tau, the major component of NTs 50 , 51 . The transcription factor SP1 also responds to inflammatory signals, such as those induced by neuronal damage.…”

Section: Discussionmentioning

confidence: 99%

Identification of oxidative stress-related genes differentially expressed in Alzheimer’s disease and construction of a hub gene-based diagnostic model

Zhang

Kiryu

2023

Sci Rep

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Alzheimer’s disease (AD) is the most prevalent dementia disorder globally, and there are still no effective interventions for slowing or stopping the underlying pathogenic mechanisms. There is strong evidence implicating neural oxidative stress (OS) and ensuing neuroinflammation in the progressive neurodegeneration observed in the AD brain both during and prior to symptom emergence. Thus, OS-related biomarkers may be valuable for prognosis and provide clues to therapeutic targets during the early presymptomatic phase. In the current study, we gathered brain RNA-seq data of AD patients and matched controls from the Gene Expression Omnibus (GEO) to identify differentially expressed OS-related genes (OSRGs). These OSRGs were analyzed for cellular functions using the Gene Ontology (GO) database and used to construct a weighted gene co-expression network (WGCN) and protein-protein interaction (PPI) network. Receiver operating characteristic (ROC) curves were then constructed to identify network hub genes. A diagnostic model was established based on these hub genes using Least Absolute Shrinkage and Selection Operator (LASSO) and ROC analyses. Immune-related functions were examined by assessing correlations between hub gene expression and immune cell brain infiltration scores. Further, target drugs were predicted using the Drug-Gene Interaction database, while regulatory miRNAs and transcription factors were predicted using miRNet. In total, 156 candidate genes were identified among 11046 differentially expressed genes, 7098 genes in WGCN modules, and 446 OSRGs, and 5 hub genes (MAPK9, FOXO1, BCL2, ETS1, and SP1) were identified by ROC curve analyses. These hub genes were enriched in GO annotations “Alzheimer’s disease pathway,” “Parkinson’s Disease,” “Ribosome,” and “Chronic myeloid leukemia.” In addition, 78 drugs were predicted to target FOXO1, SP1, MAPK9, and BCL2, including fluorouracil, cyclophosphamide, and epirubicin. A hub gene-miRNA regulatory network with 43 miRNAs and hub gene-transcription factor (TF) network with 36 TFs were also generated. These hub genes may serve as biomarkers for AD diagnosis and provide clues to novel potential treatment targets.

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“…Recent research has revealed that FOXO1 critically regulates oxidative stress-induced cellular death. It triggers apoptosis under oxidative stress and increases the expression of apoptosis-promoting genes ( Zhang et al, 2019 ). Li et al found that melatonin inhibits TM3 cells’ autophagy caused by H 2 O 2 via the AKT/FOXO1 pathway ( Li et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Melatonin alleviates ovarian function damage and oxidative stress induced by dexamethasone in the laying hens through FOXO1 signaling pathway

Bai¹,

Hao²,

Huang³

et al. 2023

Poultry Science

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Appoptosin Mediates Lesions Induced by Oxidative Stress Through the JNK-FoxO1 Pathway

Cited by 9 publications

References 59 publications

A Mutation in Endogenous saRNA miR-23a Influences Granulosa Cells Response to Oxidative Stress

A Mutation in Endogenous saRNA miR-23a Influences Granulosa Cells Response to Oxidative Stress

Identification of oxidative stress-related genes differentially expressed in Alzheimer’s disease and construction of a hub gene-based diagnostic model

Melatonin alleviates ovarian function damage and oxidative stress induced by dexamethasone in the laying hens through FOXO1 signaling pathway

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