Identification of the target gene expression of peptide SK56 in human macrophage cells during pyroptosis
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ABSTRACT:
PROVIDER: PRJNA1005651 | ENA |
REPOSITORIES: ENA
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Project description:To gain insight into the peptide SK56 target gene profile in macrophage cells, we performed RNA-seq analysis in PMA-differentiated THP-1 cells upon LPS+nigericin with or without SK56, to analyze the signaling pathway of cell pyroptosis blocked by SK56..
2023-10-22 | GSE240889 | GEO
Project description:To gain insight into the peptide SK56 target gene profile in macrophage cells, we performed RNA-seq analysis in PMA-differentiated THP-1 cells upon LPS+nigericin with or without SK56, to analyze the signaling pathway of cell pyroptosis blocked by SK56.
2024-06-21 | PXD053323 |
Project description:Macrophages are involved in the pathophysiology of many diseases as critical cells of the innate immune system. Pyroptosis is a form of macrophage death that induces cytokinesis of phagocytic substances in the macrophages, thereby defending against infection. Dimethyl itaconate (DI) is an analog of itaconic acid with anti-inflammatory effects. However, the effect of dimethyl itaconate on macrophage pyroptosis has not been elucidated clearly. Thus, the present study aimed to analyze the effect of DI treatment on a macrophage pyroptosis model (Lipopolysaccharide, LPS+Adenosine Triphosphate, ATP). The results showed that 0.25 mM DI ameliorated macrophage pyroptosis and downregulated interleukin (IL)-1β expression. Then, real-time quantitative polymerase chain reaction (RT-qPCR) was used to confirm the result of RNA-sequencing of the upregulated oxidative stress-related genes (Gclc and Gss) and downregulated inflammation-related genes (IL-12β and IL-1β). In addition, Gene Ontology (GO) enrichment analysis showed that differential genes were associated with transcript levels and DNA replication. Kyoto encyclopedia of genes and genomes (KEGG) enrichment showed that signaling pathways, such as tumor necrosis factor (TNF), Jak, Toll-like receptor and IL-17, were altered after DI treatment. N-acetyl-L-cysteine (NAC) reversed the DI effect on the LPS+ATP-induced macrophage pyroptosis and upregulated the IL-1β expression. Oxidative stress-related protein Nrf2 is involved in the DI regulation of macrophage pyroptosis. Taken together, these findings suggested that DI alleviates the pyroptosis of macrophages through oxidative stress.
2021-10-16 | GSE185895 | GEO
Project description:Immune cells play critical roles in causing host damage in various diseases, including infectious diseases. However, there is a paucity of human models to study immune-mediated host damage. Here, we systematically analyzed the changes in immune cell composition for COVID-19 pancreatic autopsy samples using the GeoMx spatial RNA and protein platform and found accumulation of proinflammatory macrophages. Single cell RNA-seq analysis of human islets upon SARS-CoV-2 or Coxsackievirus B4 (CVB4) infection identified the activation of proinflammatory macrophages and pyroptosis in β cells. To distinguish whether the virus or proinflammatory macrophages mediated β cell pyroptosis, we developed human pluripotent stem cell (hPSC)-derived vascularized macrophage-islet (VMI) organoids, containing pancreatic endocrine cells, endothelial cells, and macrophages. Both pancreatic β cells and endothelial cells in VMI organoids demonstrated improved marker expression and function compared to separately cultured cells. Additionally, proinflammatory macrophages in VMI organoids were found to induce β cell pyroptosis. Further mechanistic studies identified TNFSF12-TNFRSF12A as a contributor to proinflammatory macrophage-mediated β cell pyroptosis. Together, this study established a hPSC-derived VMI organoid as a valuable tool for studying immune cell-mediated host damage and uncovered previous unknown mechanism of β cell damage in viral infection.
2024-08-08 | GSE247805 | GEO
Project description:Immune cells play critical roles in causing host damage in various diseases, including infectious diseases. However, there is a paucity of human models to study immune-mediated host damage. Here, we systematically analyzed the changes in immune cell composition for COVID-19 pancreatic autopsy samples using the GeoMx spatial RNA and protein platform and found accumulation of proinflammatory macrophages. Single cell RNA-seq analysis of human islets upon SARS-CoV-2 or Coxsackievirus B4 (CVB4) infection identified the activation of proinflammatory macrophages and pyroptosis in β cells. To distinguish whether the virus or proinflammatory macrophages mediated β cell pyroptosis, we developed human pluripotent stem cell (hPSC)-derived vascularized macrophage-islet (VMI) organoids, containing pancreatic endocrine cells, endothelial cells, and macrophages. Both pancreatic β cells and endothelial cells in VMI organoids demonstrated improved marker expression and function compared to separately cultured cells. Additionally, proinflammatory macrophages in VMI organoids were found to induce β cell pyroptosis. Further mechanistic studies identified TNFSF12-TNFRSF12A as a contributor to proinflammatory macrophage-mediated β cell pyroptosis. Together, this study established a hPSC-derived VMI organoid as a valuable tool for studying immune cell-mediated host damage and uncovered previous unknown mechanism of β cell damage in viral infection.
2024-08-08 | GSE247808 | GEO
Project description:Immune cells play critical roles in causing host damage in various diseases, including infectious diseases. However, there is a paucity of human models to study immune-mediated host damage. Here, we systematically analyzed the changes in immune cell composition for COVID-19 pancreatic autopsy samples using the GeoMx spatial RNA and protein platform and found accumulation of proinflammatory macrophages. Single cell RNA-seq analysis of human islets upon SARS-CoV-2 or Coxsackievirus B4 (CVB4) infection identified the activation of proinflammatory macrophages and pyroptosis in β cells. To distinguish whether the virus or proinflammatory macrophages mediated β cell pyroptosis, we developed human pluripotent stem cell (hPSC)-derived vascularized macrophage-islet (VMI) organoids, containing pancreatic endocrine cells, endothelial cells, and macrophages. Both pancreatic β cells and endothelial cells in VMI organoids demonstrated improved marker expression and function compared to separately cultured cells. Additionally, proinflammatory macrophages in VMI organoids were found to induce β cell pyroptosis. Further mechanistic studies identified TNFSF12-TNFRSF12A as a contributor to proinflammatory macrophage-mediated β cell pyroptosis. Together, this study established a hPSC-derived VMI organoid as a valuable tool for studying immune cell-mediated host damage and uncovered previous unknown mechanism of β cell damage in viral infection.
2024-08-08 | GSE247807 | GEO
Project description:Immune cells play critical roles in causing host damage in various diseases, including infectious diseases. However, there is a paucity of human models to study immune-mediated host damage. Here, we systematically analyzed the changes in immune cell composition for COVID-19 pancreatic autopsy samples using the GeoMx spatial RNA and protein platform and found accumulation of proinflammatory macrophages. Single cell RNA-seq analysis of human islets upon SARS-CoV-2 or Coxsackievirus B4 (CVB4) infection identified the activation of proinflammatory macrophages and pyroptosis in β cells. To distinguish whether the virus or proinflammatory macrophages mediated β cell pyroptosis, we developed human pluripotent stem cell (hPSC)-derived vascularized macrophage-islet (VMI) organoids, containing pancreatic endocrine cells, endothelial cells, and macrophages. Both pancreatic β cells and endothelial cells in VMI organoids demonstrated improved marker expression and function compared to separately cultured cells. Additionally, proinflammatory macrophages in VMI organoids were found to induce β cell pyroptosis. Further mechanistic studies identified TNFSF12-TNFRSF12A as a contributor to proinflammatory macrophage-mediated β cell pyroptosis. Together, this study established a hPSC-derived VMI organoid as a valuable tool for studying immune cell-mediated host damage and uncovered previous unknown mechanism of β cell damage in viral infection.
2024-08-08 | GSE247806 | GEO