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RNA-Seq Analyses of the apoptosis and necroptosis in MEF

ABSTRACT: RNA-Seq Analyses of the apoptosis and necroptosis in MEF

PROVIDER: PRJNA599928 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10850809_1.fastq.gz	Fastqsanger.gz
	SRR10850809_2.fastq.gz	Fastqsanger.gz
	SRR10850810_1.fastq.gz	Fastqsanger.gz
	SRR10850810_2.fastq.gz	Fastqsanger.gz
	SRR10850811_1.fastq.gz	Fastqsanger.gz

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RNA-Seq Analyses of the apoptosis and necroptosis in MEF

Project description:Purpose: we used next generation sequencing to analyze gene expression profiles of MEF treated with PBS (control), TNF-ɑ + Cycloheximide (TC) or TNF-ɑ + Cycloheximide+ z-VAD-fmk (TCZ). The goals of this study are to compare the different gene expression profiles between MEF treated with TC compared to PBS treatment and MEF treated with TCZ compared to PBS treatment. Methods: In MEF, the combination of TNF-α and cycloheximide (TC) induces apoptosis, whereas the addition of z-VAD-fmk (TCZ) to this regimen promotes necroptosis, using High-seq 2000 Illumina sequencing platform. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays Results: By comparing the RPKM values between the two groups, a total 492 DEGs (342 upregulated and 150 downregulated) were identified in MEF treated with TC compared to PBS treatment, and a total 424 DEGs (242 upregulated and 182 downregulated) were identified in MEF treated with TCZ compared to PBS treatment. Next, we compared all identified DEGs in MEF between TC and TCZ treatment. We found that 252 DEGs overlapped between TC and TCZ treatment, whereas 240 DEGs were only present in TC treatment and 172 DEGs were only present in TCZ treatment. Conclusions: we firstly identified 492 DEGs in apoptotic MEF, and as well as 424 DEGs in necroptotic MEF. And we performed the enriched molecular pathway, molecules, transcription factors and signaling networks by IPA analysis. We revealed that apoptosis and necroptosis may share certain common canonical pathways and transcription factors.

2020-01-09 | GSE143294 | GEO

Systematic compositional analysis of extracellular vesicles produced by cells undergoing apoptosis, necroptosis or necroptosis

Project description:Systematic compositional analysis of extracellular vesicles produced by cells undergoing apoptosis, necroptosis or necroptosis

| PRJNA917299 | ENA

Systematic compositional analysis of extracellular vesicles produced by cells undergoing apoptosis, necroptosis or necroptosis

Project description:Formation of extracellular vesicles (EVs) has emerged as a novel paradigm in cell-to-cell communication in health and disease. We performed a comparative analysis of steady-state (ssEVs) and cell death-associated EVs (cdEVs) following apoptosis (apoEVs), necroptosis (necEVs), and ferroptosis (ferEVs) using the same cell line. For each EV type, we systematically determined the biophysical and biochemical characteristics, the protein cargo, and the presence of methylated ribosomal RNA. The cell death EVs showed distinctive rRNA methylation patterns compared to ssEVs.

2023-09-30 | GSE221999 | GEO

RIPK1 dephosphorylation and kinase activation by PPP1R3G/PP1γ promote apoptosis and necroptosis

Project description:Receptor-interacting protein kinase 1(RIPK1) is a key regulator of inflammation and cell death. Many sites on RIPK1, including serine 25, are phosphorylated to inhibit its kinase activity and cell death. How these inhibitory phosphorylation sites are dephosphorylated is poorly understood. Using a sensitized CRISPR whole genome knockout screen, we discover that protein phosphatase 1 regulatory subunit 3G (PPP1R3G) is required for RIPK1-dependent apoptosis and necroptosis. Mechanistically, PPP1R3G recruits its catalytic subunit protein phosphatase 1 gamma (PP1g) to Complex I to remove inhibitory phosphorylations of RIPK1. A PPP1R3G mutant which does not bind PP1g fails to rescue RIPK1 activation and cell death. Furthermore, chemical prevention of RIPK1 inhibitory phosphorylations or mutation of serine 25 of RIPK1 to alanine largely restores cell death in PPP1R3G-knockout cells. Finally, Ppp1r3g-/- mice are protected from tumor necrosis factor-induced systemic inflammatory response syndrome, confirming the important role of PPP1R3G in regulating apoptosis and necroptosis in vivo.

2021-10-26 | GSE176422 | GEO

Systematic comparative analysis of extracellular vesicles following apoptosis, necroptosis and ferroptosis

Project description:The formation of extracellular vesicles (EVs) has emerged as a novel paradigm in cell-to-cell communication during health and disease. According to the type of cell death modalities, the intercellular functions of EVs may be influenced by their biogenesis and composition. To identify a possible EV cargo signature, we performed a comparative analysis of steady-state (ssEVs) and cell death-associated EVs (cdEVs) following apoptosis (apoEVs), necroptosis (necEVs) and ferroptosis (ferEVs) in the same cell type. We determined the physical and biochemical characteristics, the protein cargo by mass spectrometry.

2023-10-12 | PXD039297 | Pride

Necroptosis of intestinal epithelial cells induces innate lymphoid cell-dependent lethal ileitis in preterm mice

Project description:CFLARs encodes short form of cellular FLICE-inhibitory protein that blocks apoptosis, but promotes necroptosis in vitro. Here, we generate transgenic mice expressing CFLARs on the X-chromosome, designated as XCFY or XCFX mice. All XCFY mice die perinatally due to severe ileitis, whereas XCFX mice appear to be normal and fertile. Intestinal epithelial cell (IEC)s of XCFY mice die by necroptosis that subsequently induces massive apoptosis of IECs. Deletion of Ripk3 or Mlkl that are essential for necroptosis rescues embryonic lethality of XCFY mice by preventing both apoptosis and necroptosis of IECs. Surprisingly, deletion of RORγt+ ILC3s or Il22 rescues embryonic lethality of CFLARs Tg mice by preventing apoptosis, but not necroptosis of IECs. Thus, necroptosis of IECs triggered by cFLIPs activates RORγt+ ILC3s, resulting in induction of lethal ileitis in preterm mice.

2019-06-21 | GSE120982 | GEO

ZBP1 is a cytosolic RNA virus sensor driving activation of the NLRP3 inflammasome, pyroptosis, necroptosis and apoptosis

Project description:The innate immune system recognizes nucleic acids as a signature of microbial infection and initiates host-protective responses, including the production of type I IFN and proinflammatory cytokines. Z-DNA binding protein 1 (ZBP1, also known as DLM-1 or DAI) was previously identified as a dsDNA binding protein, triggering DNA-mediated activation of innate immune responses. However, mice or cells lacking ZBP1 produce normal levels of type I IFN in response to dsDNA. Therefore, the classification of ZBP1 as a true DNA sensor remains to be resolved. Here, we report that the single stranded RNA virus, influenza A virus (IAV) is a trigger of the cytosolic sensor ZBP1. Sensing of IAV infection by ZBP1 engages a novel NLRP3 inflammasome pathway that is not defined by the conventions of the canonical and non-canonical NLRP3 inflammasome pathways. Surprisingly, IAV-induced cell death was not prevented by the absence of the NLRP3 inflammasome. Instead, we identified parallel contributions from pyroptosis, necroptosis and apoptosis in the execution of ZBP1-dependent cell death, mediated by the kinase RIPK3. Overall, the ability of ZBP1 to sense IAV infection signifies a point of divergence for IAV-induced programmed cell death pathways and inflammasome activation. We used microarrays to explore the gene expression profiles differentially expressed in influenza-infected bone marrow derived macrophages (BMDM) isolated from Ifnar1-/- and wild-type mice.

2016-08-11 | E-GEOD-77611 | biostudies-arrayexpress

RIPK1 dephosphorylation and kinase activation by PPP1R3G/PP1γ promote apoptosis and necroptosis

Project description:RIPK1 dephosphorylation and kinase activation by PPP1R3G/PP1γ promote apoptosis and necroptosis

| PRJNA736113 | ENA

Unexpected cross-talk between the pathogen defense mechanisms of apoptosis, necroptosis, and pyroptosis.

Project description:Unexpected cross-talk between the pathogen defense mechanisms of apoptosis, necroptosis, and pyroptosis.

| PRJNA545997 | ENA

Programmed necrosis and apoptosis differentially regulate cancer development and biliary homeostasis in the liver

Project description:For years, the term apoptosis was used synonymously for programmed cell death. However, it was recently discovered that programmed necrosis M-bM-^@M-^S dependent on the kinases Receptor-Interacting-Protein-Kinase (RIP)1 and RIP3 (also called necroptosis) M-bM-^@M-^S represents a major programmed cell-death pathway in development and immunity. At present, the functions of necroptosis in hepatitis, liver cancer development and biliary disease are unclear. Here we show that in mice with chronic hepatitis due to conditional ablation of TGF-beta-activated kinase1 (TAK1) in liver parenchymal cells (LPC), both apoptotic and necroptotic signaling pathways are activated. Strikingly, only Caspase-8-dependent apoptosis promotes spontaneous liver cancer development, while in contrast LPC necroptosis inhibits hepatic tumourigenesis. The tumour-promoting effect of apoptosis results from an induction of strong compensatory proliferation of LPC, linked with the paracrine action of growth factors like Insulin-like growth factor-2 (IGF-2) not induced by necroptosis. In addition to prevention of HCC development, induction of necroptosis leads to massive cholestasis and hyperbilirubinemia, resulting from an insufficient ductular reaction and biliary regeneration from the hepatic stem cell niche as a response to chronic hepatitis. These results indicate previously undefined distinctive functions of apoptosis and programmed necrosis in controlling cancer development and cholestasis in the liver with important implications for future therapeutic strategies in chronic liver disease. 8 samples were analysed. We compared groups of 4 Tak1/Caspase8 LPC double knockout mice and 4 Tak1 LPC-KO/Rip3-/- mice to detect genes differentially regulated by apoptotic and necrotic signalling pathways.

2013-04-01 | E-GEOD-39750 | biostudies-arrayexpress

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