LINC00894 promotes neuronal survival by regulating the expression of ATF3.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1080015 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28083213_1.fastq.gz | Fastqsanger.gz | |||
| SRR28083213_2.fastq.gz | Fastqsanger.gz | |||
| SRR28083214_1.fastq.gz | Fastqsanger.gz | |||
| SRR28083214_2.fastq.gz | Fastqsanger.gz | |||
| SRR28083215_1.fastq.gz | Fastqsanger.gz |
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Project description:There is evidence suggesting that LINC00894 may have a biological role in the brain, but the exact function of this gene remains largely unknown. In this study, we discovered that LINC00894 regulates neuronal cell apoptosis. Using RNA-seq, we identified a gene cluster regulated by LINC00894 in M17 neuroblast cell line, and qRT-PCR analysis demonstrated that LINC00894 may affect cell viability by modulating the expression of ATF3 in neuronal cells.
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Project description:Sustained activation of Wnt/β-catenin signaling has been shown to promote AKI to CKD progression. However, its underlying mechanisms remain largely unclear. In this study, we investigated this issue via unilateral ischemia/reperfusion injury in mice and hypoxia/reoxygenation (H/R) in HKC-8 cells. Both in vitro and in vivo, overexpression of Wnt1 promoted mitochondrial dynamics and mitophagy damage. Furthermore, we revealed that ATF3 not only is a transcriptional target of canonical Wnt/β-catenin signaling but is also an important pathogenic mediator of kidney disease. ATF3 was expressed in various CKD animal models, including UUO, UIRI, ADR and 5/6NX. In vitro, exogenous ATF3 induced mitochondrial dynamics and mitophagy, and silenced ATF3 expression protected mitochondrial function. Finally, compared with normal individuals, patients with various kidney diseases presented markedly elevated levels of ATF3. In addition, ATF3 levels are closely correlated with renal injury markers and renal fibrosis area in patients. Thus, these results suggest that Wnt/β-catenin/ATF3 signaling activation promotes AKI to CKD progression by regulating mitochondrial dynamics and mitophagy. ATF3 can serve as a promising potential biomarker for AKI to CKD progression.
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Project description:Sustained activation of Wnt/β-catenin signaling has been shown to promote AKI to CKD progression. However, its underlying mechanisms remain largely unclear. In this study, we investigated this issue via unilateral ischemia/reperfusion injury in mice and hypoxia/reoxygenation (H/R) in HKC-8 cells. Both in vitro and in vivo, overexpression of Wnt1 promoted mitochondrial dynamics and mitophagy damage. Furthermore, we revealed that ATF3 not only is a transcriptional target of canonical Wnt/β-catenin signaling but is also an important pathogenic mediator of kidney disease. ATF3 was expressed in various CKD animal models, including UUO, UIRI, ADR and 5/6NX. In vitro, exogenous ATF3 induced mitochondrial dynamics and mitophagy, and silenced ATF3 expression protected mitochondrial function. Finally, compared with normal individuals, patients with various kidney diseases presented markedly elevated levels of ATF3. In addition, ATF3 levels are closely correlated with renal injury markers and renal fibrosis area in patients. Thus, these results suggest that Wnt/β-catenin/ATF3 signaling activation promotes AKI to CKD progression by regulating mitochondrial dynamics and mitophagy. ATF3 can serve as a promising potential biomarker for AKI to CKD progression.
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Project description:Cardiac resident MerTK+ macrophages exert multiple protective roles post-ischemic injury, however, the mechanisms regulating their fate are not fully understood. Here we show that GAS6-inducible transcription factor ATF3 prevents apoptosis of MerTK+ macrophages after ischemia-reperfusion (IR) injury, by repressing the transcription of multiple genes involved in type I interferon expression (Ifih1 and Infb1) and apoptosis (Apaf1). Mice lacking ATF3 in cardiac macrophages or myeloid cells showed excessive loss of MerTK+ cardiac macrophages, poor angiogenesis, and worse heart dysfunction post-IR, which were rescued by the transfer of MerTK+ cardiac macrophages. GAS6 administration improved cardiac repair in an ATF3-dependent manner. Finally, we showed a negative association of GAS6 and ATF3 expression with the risk of major adverse cardiac events in patients with ischemic heart disease. These results indicate that the GAS6-ATF3 axis has a protective role against IR injury by regulating MerTK+ cardiac macrophage survival/proliferation.
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Project description:RIPK3 promotes neuronal survival by suppressing excitatory neurotransmission during CNS viral infection
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Project description:Wnt/β-catenin/ATF3 signaling promotes AKI to CKD progression by regulating mitophagy in mice [mouse]
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Project description:While recent work has identified roles for cytokines and inflammation in the regulation of neural activity, the capacity for cell intrinsic innate immune signaling within neurons to influence neurotransmission remains poorly understood. However, the existing evidence linking immune signaling with neuronal activity suggests that modulation of neurotransmission may serve previously undefined roles in host protection and pathogen control within the central nervous system. Here, we identify a specialized function for RIPK3, a kinase traditionally associated with necroptotic cell death, in preserving neuronal survival during neurotropic flavivirus infection through the suppression of excitatory neurotransmission. We show that RIPK3 coordinates transcriptomic changes in neurons that suppress neuronal glutamate signaling, thereby desensitizing neurons to excitotoxic cell death. These effects occur independently of the traditional functions of RIPK3 in promoting MLKL-dependent necroptosis and NFκB-mediated inflammatory transcription. Instead, RIPK3 promotes phosphorylation of the key neural regulatory kinase CAMKII, which in turn activates the transcription factor CREB to drive a neuroprotective transcriptional program and suppress deleterious glutamatergic signaling. These findings identify an unexpected function for a canonical cell death protein in promoting neuronal survival during viral infection through the modulation of neuronal activity, highlighting new mechanisms of neuroimmune crosstalk.
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Project description:Wnt/β-catenin/ATF3 signaling promotes AKI to CKD progression by regulating mitophagy in mice [HKC-8]
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Project description:Maintenance of genetic integrity is essential for survival of all organisms. Activating transcription factor 3 (ATF3) is a member of the c-AMP response element binding (CREB)/ATF family of transcription factors, and is highly inducible by various stress conditions including DNA damage. However, downstream targets and molecular basis underlying pleiotropic effects of ATF3 on the cell fate have been largely unknown. To identify ATF3 targets in the human genome, we carried out chromatin immunoprecipitation-microarray (ChiP-on-chip) and knockdown-expression profiling analysis using two models where ATF3 was either transiently induced or constitutively expressed. We show that ATF3 binds to an unexpectedly large number of targets; 5,984 promoters in HCT116 cells treated with an alkylating agene methyl methanesulfonate (MMS) and 1,423 promoters in LNCaP cells constitutively expressing ATF3. Importantly, targets of MMS-induced ATF3 are highly enriched not only for CREB/ATF motifs but also for binding sites of several stress sensors including DDIT3/CHOP, Egr1, and c-Ets which are concomitantly induced by MMS. Stress-induced ATF3 affects broad but select biological processes including cell cycle, cell death, adhesion, biosynthesis, and receptor signaling pathways. In addition, ATF3 binds to as many as 40% of the p53 targets and preferentially enhances MMS-induced activation of proapoptotic genes such as DR4, DR5, and PUMA, consistent with the proapoptotic effect of ATF3. These data shed new light on the co-regulatory function of ATF3 in the stress-induced transcription factor network. The comprehensive list of genomic targets of ATF3 will facilitate further understanding the role of ATF3 in determining life and death of cells under both physiological and tumour-associated stress conditions. Maintenance of genetic integrity is fundamental to survival of all organisms. DNA damage can be caused by various agents in environment and elicits complex responses in the cell. ATF3 is one of the transcription factors activated by various stress conditions including DNA damage, and has been shown to have pleiotropic effects on life and death of cells depending on the context of experimental conditions. It has been largely unknown, however, which genes and pathways are regulated by stress-induced ATF3. Here we attempted to answer this question by chromatin immunoprecipitation-microarray analysis of downstream targets of ATF3. We show that ATF3 binds to an unexpectedly large number of promoters (nearly 6,000) in a human colorectal cancer cell lineHCT116 treated with an alkylating agent methyl methanesulfonate. Interestingly, the ATF3 targets are highly enriched for binding sites of other stress sensors shedding light on a transcriptional co-regulatory network of DNA damage response. We further show that ATF3 regulates expression of genes in select biological processes including cell cycle, cell death, adhesion, metabolism, signal transduction, and the p53 pathway. The comprehensive list of ATF3 targets provides new insight into a highly inter-connected network of stress-induced transcription factors around ATF3. ChIP-chip samples: Comparison of ATF3-IP and whole genome DNA (control) Gene expression samples: HCT116 cells pre-transfected with either control siRNA or ATF3 knockdown siRNA and stimulated by methyl methanesulfonate (MMS) for 0, 6, 12, and 24 hours
2010-10-01 | E-GEOD-18457 | biostudies-arrayexpress