Transcriptional changes and RNA expression profiles during ischemia-induced DRP1-mediated macrophage reprogramming
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PROVIDER: PRJNA1176845 | ENA |
REPOSITORIES: ENA
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Project description:To reveal the molecular mechanisms underlying DRP1-mediated macrophage reprogramming during hypoxia serum starvation (HSS) an in vitro ischemia model, we performed bulk RNA-seq analysis on mouse bone marrow derived macrophages (BMDM) upon HSS-induced DRP1 mediated macrophage reprogramming.
2024-10-28 | GSE280186 | GEO
Project description:Purpose:to verify Drp1-mediated biological pathways under physiological and ischemia conditions.Methods:C57BL/6 mice and Drp1 knockdown mice were used for ischemia treatment. Right femoral arteries were catheterized with polyethylene catheters for bleeding 50% of total blood volume (≈7% of weight). The ischemia time started to calculate after the model was established. A laparotomy was then carried out to obtain superior mesenteric artery tissues (SMAs) for transcriptome analysis. Series-Cluster analysis was performed to identify the global trends of mitochondrial DEGs after Drp1 knockdown. Gene ontology (GO) analysis was performed to facilitate elucidating the biological process (BP), molecular function (MF) and cellular component (CC) of unique genes in the significant or representative profiles. Results:In addition to its traditional roles in GTPase regulation and mitochondrial fission, Drp1 may also regulate actin cytoskeleton and the movement of microtubules. Besides, Drp1 may participate in the regulation of morphology and functions of other organelles, including endoplasmic reticulum, peroxisome, phagolysosome, etc. As for general organ functions, Drp1 may regulate vascular constriction and dilation. These consequences indicated the important role of Drp1 in ischemia-induced cellular regulation. Conclusions: Drp1 deficiency proves the important role of Drp1 in ischemia-induced biomedical processes through multiple potential fission-independent manners. Methods:C57BL/6 mice and Drp1 knockdown mice were used for ischemia treatment. Right femoral arteries were catheterized with polyethylene catheters for bleeding 50% of total blood volume (≈7% of weight). The ischemia time started to calculate after the model was established. A laparotomy was then carried out to obtain superior mesenteric artery tissues (SMAs) for transcriptome analysis. Series-Cluster analysis was performed to identify the global trends of mitochondrial DEGs after Drp1 knockdown. Gene ontology (GO) analysis was performed to facilitate elucidating the biological process (BP), molecular function (MF) and cellular component (CC) of unique genes in the significant or representative profiles. Results:In addition to its traditional roles in GTPase regulation and mitochondrial fission, Drp1 may also regulate actin cytoskeleton and the movement of microtubules. Besides, Drp1 may participate in the regulation of morphology and functions of other organelles, including endoplasmic reticulum, peroxisome, phagolysosome, etc. As for general organ functions, Drp1 may regulate vascular constriction and dilation. These consequences indicated the important role of Drp1 in ischemia-induced cellular regulation. Conclusions: Drp1 deficiency proves the important role of Drp1 in ischemia-induced biomedical processes through multiple potential fission-independent manners.
2020-04-29 | GSE124096 | GEO
Project description:Transcriptome Analysis of Drp1-mediated biological pathways under physiological and ischemia conditions in Drp1-knockdown mice
| PRJNA510759 | ENA
Project description:We performed RNAseq analysis of 3 days in vitro activated control and Drp1 KO T cells to investigate the role of Drp1 in regulating global transcriptional changes upon activation in T cells. Our analysis shows that Drp1 sustains metabolic reprogramming upon TCR stimulation. Indeed, in Drp1 KO T cells most of the genes encoding for glycolytic enzymes are down-regulated, while TCA cycle and oxidative phosphorylation genes, as well as several genes encoding enzymes of fatty acid synthesis and beta-oxidation, are upregulated.
2018-12-11 | GSE112143 | GEO
Project description:Macrophages play a critical role in the regulation of inflammation and tissue homeostasis. In addition to their vital functions for cell survival and physiology, mitochondria play a crucial role in innate immunity as a platform for the induction of inflammatory responses by regulating cell signaling and dynamics. Dynamin-related protein 1 (Drp1) plays a role in the induction of inflammatory responses and the subsequent development of various diseases. PGAM5 (phosphoglycerate mutase member 5) is a mitochondrial outer membrane phosphatase that dephosphorylates its substrate, Drp1. Previous studies showed that PGAM5 regulates the phosphorylation of Drp1 for the activation of NKT cells and T cells. However, it is not clear how PGAM5 regulates Drp1 activity for the induction of inflammation in macrophages. Here, we demonstrate that PGAM5 activity regulates the dephosphorylation of Drp1 in macrophages, leading to the induction of proinflammatory responses in macrophages. In TLR signaling, PGAM5 regulates the expression and production of inflammatory cytokines by regulating the activation of downstream signaling pathways, including the NF-kB and MAPK pathways. Upon LPS stimulation, PGAM5 interacts with Drp1 to form a complex, leading to the production of mtROS. Furthermore, PGAM5-Drp1 signaling promotes the polarization of macrophages toward a proinflammatory phenotype. Our study further demonstrates that PGAM5-Drp1 signaling promotes metabolic reprogramming by upregulating glycolysis and mitochondrial metabolism in macrophages. Altogether, PGAM5 signaling might be a link between alterations in Drp1-mediated mitochondrial dynamics and inflammatory responses in macrophages and may be a target for the treatment of inflammatory diseases.
2023-06-20 | GSE235306 | GEO
Project description:Macrophages are a heterogeneous cell type implicated in injury, repair, and fibrosis after AKI, but the macrophage population associated with each phase is unclear.results of this study in a renal ischemia-reperfusion injury model allow phenotype and function to be assigned to CD11b+/Ly6C+ monocyte/macrophage populations in the pathophysiology of disease after AKI. we used a renal bilateral ischemia-reperfusion injury mouse model to identify unique monocyte/macrophage populations by differential expression of Ly6C in CD11b+Â cells and to define the function of these cells in the pathophysiology of disease on the basis of microarray gene signatures and reduction strategies Macrophage populations were sorted by Flow Cytometry into low and intermediate populations by Itgam(Cd11b) and Ly6c markers. The cells obtained in 5 weeks sham, 5 weeks IR, 9 day sham, and 9 day IR with 6 samples per group (3 int and 3 low). Cells were sorted in 350ul of RLT lysing buffer and kept at -80c until RNA extraction.Sample amplification, fragmentation, hybridization,washing and scanning were performed according to validated Affymetrix protocol in a CLIA certified lab.
2015-12-09 | E-GEOD-75808 | biostudies-arrayexpress
Project description:HDC/histamine signaling axis drives macrophage reprogramming to promote angiogenesis in the hindlimb ischemia mice
| PRJNA1142941 | ENA
Project description:Macrophages are a heterogeneous cell type implicated in injury, repair, and fibrosis after AKI, but the macrophage population associated with each phase is unclear.results of this study in a renal ischemia-reperfusion injury model allow phenotype and function to be assigned to CD11b+/Ly6C+ monocyte/macrophage populations in the pathophysiology of disease after AKI. we used a renal bilateral ischemia-reperfusion injury mouse model to identify unique monocyte/macrophage populations by differential expression of Ly6C in CD11b+ cells and to define the function of these cells in the pathophysiology of disease on the basis of microarray gene signatures and reduction strategies
2015-12-09 | GSE75808 | GEO
Project description:Molecular changes caused by metabolic reprogramming in ischemia and reperfusion cortex remain an unaddressed issue. Applying the quantitative proteomic and lactylproteomic analysis, we found that the molecular changes of ischemic brain tissues are quite different between ischemia and reperfusion stages. Conjoint analysis with a previous published transcriptome data further showed that the significant changes in protein levels and protein lactylations were mainly correlated with neurons in the reperfusion and ischemia stages, respectively. The significant upregulated lactylation of Aldoc, one of the glycolytic enzymes, at lysine 230 may contribute to the metabolic reprogramming by regulating glycolysis of astrocyte in ischemia phase, and which may further promote the lactate-derived lactylation of protein lysine residues. Our findings lay the foundation for future mechanistic studies of metabolic reprogramming from a novel perspective of lactylation, and illustrate that protein lactylations may play important roles in regulating the biological functions of neural cells after ischemic stroke.
2024-10-17 | PXD019323 | Pride
Project description:Macrophage histone lactylation during ischemia induced-muscle regeneration
| PRJNA1068601 | ENA