Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA263168 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MEFs were grown from WT and PDPN-deficient mouse embryos and gene expression was analyzed. The aim was to determine whether a lack of PDPN caused significant global changes in gene expression in primary fibroblasts. Here, we performed a microarray on WT and PDPN-deficient mouse embryonic fibroblasts to determine whether there were signficiant underlying changes in gene expression. Two replicates each of WT and PDPN KO MEFs from C57BL6/J mice
2014-10-07 | E-GEOD-62081 | biostudies-arrayexpress
Project description:MEFs were grown from WT and PDPN-deficient mouse embryos and gene expression was analyzed. The aim was to determine whether a lack of PDPN caused significant global changes in gene expression in primary fibroblasts. Here, we performed a microarray on WT and PDPN-deficient mouse embryonic fibroblasts to determine whether there were signficiant underlying changes in gene expression.
2014-10-07 | GSE62081 | GEO
Project description:Whole genome expression data comparison between WT and Cebpg-/- MEFs.
2015-07-17 | E-GEOD-47777 | ExpressionAtlas
Project description:Gene expression in WT and Ikaros-deficient LSK cells
2016-01-08 | E-GEOD-61147 | ExpressionAtlas
Project description:The effect of Podoplanin (Pdpn) expression on the differential expression profile of RAW264.7 cells has been characterised in wildtype, Pdpn knockout cells and Pdpn overexpressed cells before and after H. pylori infection using 770 genes from the NanoString Mouse PanCancer Pathways Panel.
2020-05-28 | GSE151269 | GEO
Project description:Microarray analysis of gene expression in ATM-deficient MEFs
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Project description:Total Gene expression analysis of H3f3b null and WT MEFs
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Project description:The macrophage response to infected microbes is crucial for the development of life-threatening sepsis. However, the mechanisms underlying pathophysiological regulation of macrophage subsets during sepsis remain poorly understood. Here, we report a novel mechanism in which the adhesion and degranulation-promoting adapter protein (ADAP) is essential for priming macrophages to induce podoplanin (PDPN) in response to bacterial infection during sepsis. We showed that ADAP expression was robustly induced in macrophages following LPS stimulation and was associated with sepsis severity. Furthermore, PDPN failed to be upregulated in TLR4 stimulated macrophages deficient in ADAP. A distinct PDPNhi peritoneal macrophage (PM) subset, which exhibited an M2-like phenotype and enhanced phagocytic activity, was generated in WT but not in ADAP-deficient septic mice. The blockade of PDPNhi PMs mimicked the effect of ADAP deficiency, which exacerbated sepsis. Mechanistically, BTK-mediated ADAP Y571 phosphorylation worked together with mTOR to converge on STAT3 activation for the transactivation of the PDPN promoter. Moreover, agonist activation of STAT3 profoundly potentiated the PDPNhi PM subset generation and alleviated sepsis severity in mice. Together, our findings reveal a novel mechanism whereby ADAP resets macrophage function by controlling the TLR4-induced upregulation of PDPN as a host innate immune defense during sepsis.
2025-01-10 | GSE281049 | GEO
Project description:The macrophage response to infected microbes is crucial for the development of life-threatening sepsis. However, the mechanisms underlying pathophysiological regulation of macrophage subsets during sepsis remain poorly understood. Here, we report a novel mechanism in which the adhesion and degranulation-promoting adapter protein (ADAP) is essential for priming macrophages to induce podoplanin (PDPN) in response to bacterial infection during sepsis. We showed that ADAP expression was robustly induced in macrophages following LPS stimulation and was associated with sepsis severity. Furthermore, PDPN failed to be upregulated in TLR4 stimulated macrophages deficient in ADAP. A distinct PDPNhi peritoneal macrophage (PM) subset, which exhibited an M2-like phenotype and enhanced phagocytic activity, was generated in WT but not in ADAP-deficient septic mice. The blockade of PDPNhi PMs mimicked the effect of ADAP deficiency, which exacerbated sepsis. Mechanistically, BTK-mediated ADAP Y571 phosphorylation worked together with mTOR to converge on STAT3 activation for the transactivation of the PDPN promoter. Moreover, agonist activation of STAT3 profoundly potentiated the PDPNhi PM subset generation and alleviated sepsis severity in mice. Together, our findings reveal a novel mechanism whereby ADAP resets macrophage function by controlling the TLR4-induced upregulation of PDPN as a host innate immune defense during sepsis.
2025-01-10 | GSE281047 | GEO
Project description:The macrophage response to infected microbes is crucial for the development of life-threatening sepsis. However, the mechanisms underlying pathophysiological regulation of macrophage subsets during sepsis remain poorly understood. Here, we report a novel mechanism in which the adhesion and degranulation-promoting adapter protein (ADAP) is essential for priming macrophages to induce podoplanin (PDPN) in response to bacterial infection during sepsis. We showed that ADAP expression was robustly induced in macrophages following LPS stimulation and was associated with sepsis severity. Furthermore, PDPN failed to be upregulated in TLR4 stimulated macrophages deficient in ADAP. A distinct PDPNhi peritoneal macrophage (PM) subset, which exhibited an M2-like phenotype and enhanced phagocytic activity, was generated in WT but not in ADAP-deficient septic mice. The blockade of PDPNhi PMs mimicked the effect of ADAP deficiency, which exacerbated sepsis. Mechanistically, BTK-mediated ADAP Y571 phosphorylation worked together with mTOR to converge on STAT3 activation for the transactivation of the PDPN promoter. Moreover, agonist activation of STAT3 profoundly potentiated the PDPNhi PM subset generation and alleviated sepsis severity in mice. Together, our findings reveal a novel mechanism whereby ADAP resets macrophage function by controlling the TLR4-induced upregulation of PDPN as a host innate immune defense during sepsis.
2025-01-10 | GSE281052 | GEO