ZFP36 protects against oxygen-glucose deprivation/reoxygenation-induced mitochondrial fragmentation and neuronal apoptosis through inhibiting NOX4-DRP1 pathway

Guo, Hengjiang; Jiang, Yan; Gu, Zhiqing; Ren, Li; Zhu, Change; Yu, Shiying; Rong, Wei

doi:10.1016/j.brainresbull.2021.12.003

Cited by 13 publications

(7 citation statements)

References 44 publications

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“…The well-known immune gene ZFP36 (MCMCglmm: solitary, post mean = 1.07, pMCMC = 0.02; longevity, post mean = 2.21 ± 0.07, pMCMC = 0.02 ± 5.05 × 10 −3 ) modulates anti-viral immunity by controlling T cell activation 39 and protects against inflammatory diseases through regulating inflammatory cytokines, such as TNF-α 40 , 41 . ZFP36 also plays a role in neuroprotection and inhibits neuronal apoptosis 42 . Another gene of interest was XRCC6 (MCMCglmm: solitary, post mean = −1.50, pMCMC = 3.33 × 10 −3 , Fig.…”

Section: Resultsmentioning

confidence: 99%

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Correlated evolution of social organization and lifespan in mammals

et al. 2023

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Discerning the relationship between sociality and longevity would permit a deeper understanding of how animal life history evolved. Here, we perform a phylogenetic comparative analysis of ~1000 mammalian species on three states of social organization (solitary, pair-living, and group-living) and longevity. We show that group-living species generally live longer than solitary species, and that the transition rate from a short-lived state to a long-lived state is higher in group-living than non-group-living species, altogether supporting the correlated evolution of social organization and longevity. The comparative brain transcriptomes of 94 mammalian species identify 31 genes, hormones and immunity-related pathways broadly involved in the association between social organization and longevity. Further selection features reveal twenty overlapping pathways under selection for both social organization and longevity. These results underscore a molecular basis for the influence of the social organization on longevity.

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Section: Resultsmentioning

confidence: 99%

“…ZFP36 also plays a role in neuroprotection and inhibits neuronal apoptosis 42 . Another gene of interest was XRCC6 (MCMCglmm: solitary, post mean = −1.50, pMCMC = 3.33 × 10 −3 , Fig.…”

Section: Gene Expression Of Social Organization and Longevitymentioning

confidence: 99%

Correlated evolution of social organization and lifespan in mammals

et al. 2023

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“…It degrades Tnf, Ptgs2, and Ccl3 mRNAs and negatively regulates NF-κB signaling at the transcriptional corepressor level [26] [27] [28] [29]. Recently, Zfp36 was reported to be increased in immortalized hippocampal HT22 neuronal cells after oxygen-glucose deprivation/reoxygenation treatment, and it protects against mitochondrial fragmentation and neuronal apoptosis [30]. In our mouse MCAO models, Zfp36 was upregulated in permanent MCAO, but not in transient MCAO; thus, we speculate that study on the regulation of in ammation by Zfp36 after brain ischemia may be a promising future research direction.…”

Section: Discussionmentioning

confidence: 99%

Re-Exploring the Inflammation-Related Core Genes and Modules in Cerebral Ischemia

Jiang

et al. 2023

Mol Neurobiol

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The genetic transcription pro le of brain ischemic and reperfusion injury remains elusive. To address this, we used an integrative analysis approach including differentially expressed genes (DEGs) analysis, weighted-gene co-expression network analysis (WGCNA), and pathway and biological processes analysis to analyze data from the microarray studies of nine mice and ve rats after middle cerebral artery occlusion (MCAO), and six primary cell transcriptional datasets in the Gene Expression Omnibus (GEO). We identi ed reperfusion as the main confounding factor in gene pro le changes. Our analyses of pathway and biological processes revealed upregulated functional modules involved in in ammatory disequilibrium and thrombus formation. Astrocytes, microglia, and macrophages were the main contributors of in ammation-related gene changes. Novel core hubs implicated in negative regulation of in ammation (Zfp36, Nfkbiz, and Maff) were identi ed and validated. Collectively, these results expand our knowledge of the genetic pro le involved in brain ischemia and reperfusion, highlighting the crucial role of in ammatory disequilibrium in brain ischemia.

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“…Zfp36, HMOX1, and ATF3 have antioxidant effects and play important roles in tumor progression. Zfp36, also known as tristetraprolin, has a neuroprotective effect and protects dopaminergic neurons from oxidative damage [ 37 ]. However, unlike Zfp36, HMOX1 has a dual role in tumor cells.…”

Section: Discussionmentioning

confidence: 99%

In Silico Analysis of Ferroptosis-Related Genes and Its Implication in Drug Prediction against Fluorosis

Liu

et al. 2023

IJMS

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Fluorosis is a serious global public health problem. Interestingly, so far, there is no specific drug treatment for the treatment of fluorosis. In this paper, the potential mechanisms of 35 ferroptosis-related genes in U87 glial cells exposed to fluoride were explored by bioinformatics methods. Significantly, these genes are involved in oxidative stress, ferroptosis, and decanoate CoA ligase activity. Ten pivotal genes were found by the Maximal Clique Centrality (MCC) algorithm. Furthermore, according to the Connectivity Map (CMap) and the Comparative Toxicogenomics Database (CTD), 10 possible drugs for fluorosis were predicted and screened, and a drug target ferroptosis-related gene network was constructed. Molecular docking was used to study the interaction between small molecule compounds and target proteins. Molecular dynamics (MD) simulation results show that the structure of the Celestrol–HMOX1 composite is stable and the docking effect is the best. In general, Celastrol and LDN-193189 may target ferroptosis-related genes to alleviate the symptoms of fluorosis, which may be effective candidate drugs for the treatment of fluorosis.

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ZFP36 protects against oxygen-glucose deprivation/reoxygenation-induced mitochondrial fragmentation and neuronal apoptosis through inhibiting NOX4-DRP1 pathway

Cited by 13 publications

References 44 publications

Correlated evolution of social organization and lifespan in mammals

Correlated evolution of social organization and lifespan in mammals

Re-Exploring the Inflammation-Related Core Genes and Modules in Cerebral Ischemia

In Silico Analysis of Ferroptosis-Related Genes and Its Implication in Drug Prediction against Fluorosis

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