Cold-inducible RNA-binding protein inhibits neuron apoptosis through the suppression of mitochondrial apoptosis

Zhang, Haitao; Xue, Jun; Zhang, Zhiwen; Kong, Haibo; Liu, Aijun; Li, Shouchun; Xu, Donggang

doi:10.1016/j.brainres.2015.07.004

Cited by 47 publications

(44 citation statements)

References 27 publications

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“…Sakurai et al observed that mild hypothermia-induced elevated CIRP levels inhibited tumor necrosis factor-alphainduced apoptosis by caspase-8 activation and ERK phosphorylation [30]. Zhang et al revealed a neuroprotective effect of CIRBP during mild hypothermia by inhibiting neuron apoptosis via the suppression of the mitochondria apoptosis pathway [14]. Consistent with these previous reports, we found that CIRBP overexpression significantly attenuated Aβ-induced neuronal apoptosis and exerted a neuroprotective effect in cultured rat cortical neurons.…”

Section: Discussionsupporting

confidence: 91%

“…In response to stress, CIRBP generally modulates mRNA stability at the posttranscriptional level through its binding site on the 3′untranslational region (UTR) of its targeted mRNAs [12,13]. Recent studies have demonstrated that CIRBP exerts neuroprotective effects against H 2 O 2 -induced cell death through the Akt and ERK pathways in primary rat cortical neurons and neuro2a (N2a) cells [14][15][16]. The aim of the present study is to investigate how CIRBP reacts to the intracellular and extracellular Aβ treatment, and whether CIRBP can protect against Aβ-induced toxicity in cultured rat primary cortical neurons.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

CIRBP Ameliorates Neuronal Amyloid Toxicity via Antioxidative and Antiapoptotic Pathways in Primary Cortical Neurons

Yang

Wang

et al. 2020

Oxidative Medicine and Cellular Longevity

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It is generally accepted that the amyloid β (Aβ) peptide toxicity contributes to neuronal loss and is involved in the initiation and progression of Alzheimer’s disease (AD). Cold-inducible RNA-binding protein (CIRBP) is reported to be a general stress-response protein, which is induced by different stress conditions. Previous reports have shown the neuroprotective effects of CIRBP through the suppression of apoptosis via the Akt and ERK pathways. The objective of this study is to examine the effect of CIRBP against Aβ-induced toxicity in cultured rat primary cortical neurons and attempt to uncover its underlying mechanism. Here, MTT, LDH release, and TUNEL assays showed that CIRBP overexpression protected against both intracellular amyloid β- (iAβ-) induced and Aβ25-35-induced cytotoxicity in rat primary cortical neurons. Electrophysiological changes responsible for iAβ-induced neuronal toxicity, including an increase in neuronal resting membrane potentials and a decrease in K+ currents, were reversed by CIRBP overexpression. Western blot results further showed that Aβ25-35 treatment significantly increased the level of proapoptotic protein Bax, cleaved caspase-3, and cleaved caspase-9 and decreased the level of antiapoptotic factor Bcl-2, but were rescued by CIRBP overexpression. Furthermore, CIRBP overexpression prevented the elevation of ROS induced by Aβ25-35 treatment by decreasing the activities of oxidative biomarker and increasing the activities of key enzymes in antioxidant system. Taken together, our findings suggested that CIRBP exerted protective effects against neuronal amyloid toxicity via antioxidative and antiapoptotic pathways, which may provide a promising candidate for amyloid-based AD prevention or therapy.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

CIRBP Ameliorates Neuronal Amyloid Toxicity via Antioxidative and Antiapoptotic Pathways in Primary Cortical Neurons

Yang

Wang

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

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“…Past studies have demonstrated that CIRBP proteins regulate cell fate by inhibiting pro-apoptotic pathways during newt spermatogenesis (Eto et al, 2009) and in the mammalian nervous system (Zhang et al, 2015). To further explore an anti-apoptotic role for axolotl cirbp in limb regeneration, we delivered a translation-blocking morpholino to early blastemas (Figure S2), and assayed cell death using TUNEL staining 4 days later.…”

Section: Resultsmentioning

confidence: 99%

A Tissue-Mapped Axolotl De Novo Transcriptome Enables Identification of Limb Regeneration Factors

et al. 2017

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SUMMARY Mammals have extremely limited regenerative capabilities; however, axolotls are profoundly regenerative and can replace entire limbs. The mechanisms underlying limb regeneration remain poorly understood, partly because the enormous and incompletely sequenced genomes of axolotls have hindered the study of genes facilitating regeneration. We assembled and annotated a de novo transcriptome using RNA-sequencing profiles for a broad spectrum of tissues that is estimated to have near-complete sequence information for 88% of axolotl genes. We devised expression analyses that identified the axolotl orthologs of cirbp and kazald1 as highly expressed and enriched in blastemas. Using morpholino anti-sense oligonucleotides, we find evidence that cirbp plays a cytoprotective role during limb regeneration while manipulation of kazald1 expression disrupts regeneration. Our transcriptome and annotation resources greatly complement previous transcriptomic studies and will be a valuable resource for future research in regenerative biology.

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“…In vitro , CIRP and RBM3 function against apoptosis in neurons 55, 56 . Hypothermia-induced CIRP expression also protects hepatocytes in fulminant hepatitis by reducing ROS production 57 .…”

Section: Discussionmentioning

confidence: 99%

TRPV4-dependent induction of a novel mammalian cold-inducible protein SRSF5 as well as CIRP and RBM3

Fujita

Higashitsuji

Liu

et al. 2017

Sci Rep

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Cold-inducible RNA-binding protein (CIRP) and RNA-binding motif protein 3 (RBM3) are two evolutionarily conserved RNA-binding proteins that are structurally related to hnRNPs and upregulated in response to moderately low temperatures in mammalian cells. Although contributions of splicing efficiency, the gene promoters activated upon mild hypothermia and the transcription factor Sp1 to induction of CIRP have been reported, precise mechanisms by which hypothermia and other stresses induce the expression of mammalian cold-inducible proteins (CIPs) are poorly understood. By screening the serine/arginine-rich splicing factors (SRSFs), we report that the transcript and protein levels of SRSF5 were increased in mammalian cells cultured at 32 °C. Expression of SRSF5 as well as CIRP and RBM3 were also induced by DNA damage, hypoxia, cycloheximide and hypotonicity. Immunohistochemical studies demonstrated that SRSF5 was constitutively expressed in male germ cells and the level was decreased in human testicular germ cell tumors. SRSF5 facilitated production of p19 H-RAS, and increased sensitivity to doxorubicin in human U-2 OS cells. Induction of CIPs was dependent on transient receptor potential vanilloid 4 (TRPV4) channel protein, but seemed independent of its ion channel activity. These findings indicate a previously unappreciated role for the TRP protein in linking environmental stress to splicing.

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Cold-inducible RNA-binding protein inhibits neuron apoptosis through the suppression of mitochondrial apoptosis

Cited by 47 publications

References 27 publications

CIRBP Ameliorates Neuronal Amyloid Toxicity via Antioxidative and Antiapoptotic Pathways in Primary Cortical Neurons

CIRBP Ameliorates Neuronal Amyloid Toxicity via Antioxidative and Antiapoptotic Pathways in Primary Cortical Neurons

A Tissue-Mapped Axolotl De Novo Transcriptome Enables Identification of Limb Regeneration Factors

TRPV4-dependent induction of a novel mammalian cold-inducible protein SRSF5 as well as CIRP and RBM3

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