Lactobacillus pentosus Alleviates Lipopolysaccharide-Induced Neuronal Pyroptosis via Promoting BIRC3-Mediated Inactivation of NLRC4

Hu, Ming; Shao, Zhongying

doi:10.1155/2022/2124876

Cited by 4 publications

(3 citation statements)

References 37 publications

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“…Among these genes, YWAHZ and BIRC3 were most heavily weighted in the hazard model. It was suggested that overexpression of YWAHZ and BIRC3 could inhibit the pyroptosis [20,21] . Pyroptosis is a pro-in ammatory cell death, which could be triggered by proin ammatory factors, including Interleukin-1β (IL-1β),IL-6 [22] .During pyroptosis process, the GSDMD was cleaved by the in ammatory caspases in the tumor, which played important roles in the pyroptosis [23] .…”

Section: Discussionmentioning

confidence: 99%

Identification of the prognosis value of pyroptosis related genes in the NSCLC

Huang,

Fan,

et al. 2024

Preprint

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Backgrounds:Our study aimed to identify the prognosis value of pyroptosis related genes of cancer associated fibroblasts (CAFs) in the NSCLC. Methods:We downloaded series matrix file data of GSE117570 from the NCBI GEO public database for single cell analysis. And the GSE30219, GSE37745 were used for verification. Furthermore, we downloaded the raw mRNA expression data of processed Lung adenocarcinoma (LUAD) including normal group (n=59), tumor group (n=541) from the TCGA database (https://portal.gdc.cancer.gov/).We performed gene set enrichment analysis (GSEA) and gene set variant analysis (GSVA) for the pyroptosis-related genes. Then we constructed the risk model using the pyroptosis related genes and identify the difference signature of the CAFs between the high risk group and low risk group. Nomogram and Kaplan–Meier method were used to validate the prognostic value of risk model. Results:We constructed a risk model using the GGA2, TLR2, PKM , CALM3, RBBP7, CAPNS1, YWHAZ and BIRC3. GSEA results showed that carbon metabolism, galactose metabolism, and p53 signaling pathways were all involved. The results of GSVA showed that the differences between patients were mainly enriched in signaling pathways such as mTORC1 signaling. The T cells CD8, Macrophages M0, Macrophages M1 were significantly higher in the high risk group. The expression levels of 8 model genes were significantly correlated with the expression levels of multiple tumor-related genes. BIRC3 and ATM are significantly positively correlated. Conclusions:The pyroptosis of the CAFs are related to the prognosis of the NSCLC.

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Section: Discussionmentioning

confidence: 99%

Identification of the prognosis value of pyroptosis related genes in the NSCLC

Huang,

Fan,

et al. 2024

Preprint

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“…The literature reports that Birc3 expression is associated with tumor prognosis, inflammatory response and immune disorders ( 27 – 29 ). Birc3 inhibits cellular pyroptosis by inactivating NLRC4 inflammatory vesicles ( 30 ).…”

Section: Discussionmentioning

confidence: 99%

Novel ceRNA network construction associated with programmed cell death in acute rejection of heart allograft in mice

Guo,

Zhang,

et al. 2023

Front. Immunol.

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BackgroundT cell-mediated acute rejection(AR) after heart transplantation(HT) ultimately results in graft failure and is a common indication for secondary transplantation. It’s a serious threat to heart transplant recipients. This study aimed to explore the novel lncRNA-miRNA-mRNA networks that contributed to AR in a mouse heart transplantation model.MethodsThe donor heart from Babl/C mice was transplanted to C57BL/6 mice with heterotopic implantation to the abdominal cavity. The control group was syngeneic heart transplantation with the same kind of mice donor. The whole-transcriptome sequencing was performed to obtain differentially expressed mRNAs (DEmRNAs), miRNAs (DEmiRNAs) and lncRNAs (DElncRNAs) in mouse heart allograft. The biological functions of ceRNA networks was analyzed by GO and KEGG enrichment. Differentially expressed ceRNA involved in programmed cell death were further verified with qRT-PCR testing.ResultsLots of DEmRNAs, DEmiRNAs and DElncRNAs were identified in acute rejection and control after heart transplantation, including up-regulated 4754 DEmRNAs, 1634 DElncRNAs, 182 DEmiRNAs, and down-regulated 4365 DEmRNAs, 1761 DElncRNAs, 132 DEmiRNAs. Based on the ceRNA theory, lncRNA-miRNA-mRNA regulatory networks were constructed in allograft acute rejection response. The functional enrichment analysis indicate that the down-regulated mRNAs are mainly involved in cardiac muscle cell contraction, potassium channel activity, etc. and the up-regulated mRNAs are mainly involved in T cell differentiation and mononuclear cell migration, etc. The KEGG pathway enrichment analysis showed that the down-regulated DEmRNAs were mainly enriched in adrenergic signaling, axon guidance, calcium signaling pathway, etc. The up-regulated DEmRNAs were enriched in the adhesion function, chemokine signaling pathway, apoptosis, etc. Four lncRNA-mediated ceRNA regulatory pathways, Pvt1/miR-30c-5p/Pdgfc, 1700071M16Rik/miR-145a-3p/Pdgfc, 1700071M16Rik/miR-145a-3p/Tox, 1700071M16Rik/miR-145a-3p/Themis2, were finally validated. In addition, increased expression of PVT1, 1700071M16Rik, Tox and Themis2 may be considered as potential diagnostic gene biomarkers in AR.ConclusionWe speculated that Pvt1/miR-30c-5p/Pdgfc, 1700071M16Rik/miR-145a-3p/Pdgfc, 1700071M16Rik/miR-145a-3p/Tox and 1700071M16Rik/miR-145a-3p/Themis2 interaction pairs may serve as potential biomarkers in AR after HT.

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“…To isolate pyroptosis, we treated cells with LPS, flagellin, or a mixture of LPS and nigericin. [40][41][42][43][44][45] To isolate apoptosis, we treated cells with hydrogen peroxide (H2O2) and thapsigargin. 44,[46][47][48][49] In addition, we also incubated some wells with apoptotic and pyroptotic inhibitors prior to treatment.…”

Section: Experimental Design and Cell Death Process Validationmentioning

confidence: 99%

A morphology and secretome map of pyroptosis

Lippincott,

Tomkinson,

Bunten

et al. 2024

Preprint

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Pyroptosis represents one type of Programmed Cell Death (PCD). It is a form of inflammatory cell death that is canonically defined by caspase-1 cleavage and Gasdermin-mediated membrane pore formation. Caspase-1 initiates the inflammatory response (through IL-1β processing), and the N-terminal cleaved fragment of Gasdermin D polymerizes at the cell periphery forming pores to secrete pro-inflammatory markers. Cell morphology also changes in pyroptosis, with nuclear condensation and membrane rupture. However, recent research challenges canon, revealing a more complex secretome and morphological response in pyroptosis, including overlapping molecular characterization with other forms of cell death, such as apoptosis. Here, we take a multimodal, systems biology approach to characterize pyroptosis. We treated human Peripheral Blood Mononuclear Cells (PBMCs) with 36 different combinations of stimuli to induce pyroptosis or apoptosis. We applied both secretome profiling (nELISA) and high-content fluorescence microscopy (Cell Painting). To differentiate apoptotic, pyroptotic and healthy cells, we used canonical secretome markers and modified our Cell Painting assay to mark the N-terminus of Gasdermin-D. We trained hundreds of machine learning (ML) models to reveal intricate morphology signatures of pyroptosis that implicate changes across many different organelles and predict levels of many pro-inflammatory markers. Overall, our analysis provides a detailed map of pyroptosis which includes overlapping and distinct connections with apoptosis revealed through a mechanistic link between cell morphology and cell secretome.

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Lactobacillus pentosus Alleviates Lipopolysaccharide-Induced Neuronal Pyroptosis via Promoting BIRC3-Mediated Inactivation of NLRC4

Cited by 4 publications

References 37 publications

Identification of the prognosis value of pyroptosis related genes in the NSCLC

Identification of the prognosis value of pyroptosis related genes in the NSCLC

Novel ceRNA network construction associated with programmed cell death in acute rejection of heart allograft in mice

A morphology and secretome map of pyroptosis

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