Wildtype and NRP1 knockout macrophages
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA433729 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6705532.fastq.gz | Fastqsanger.gz |
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Project description:Obesity gives rise to metabolic complications by mechanisms that are poorly understood. While chronic inflammatory signaling in adipose tissue is typically associated with metabolic deficiencies linked to excessive weight gain, we identified a subset of NRP1-expressing myeloid cells that accumulate in adipose tissue and protect against obesity and metabolic syndrome. Ablation of NRP1 in macrophages compromised lipid uptake in these cells, which reduced substrates for fatty acid β-oxidation and shifted energy metabolism of these macrophages towards a more inflammatory glycolytic metabolism. Conditional deletion of NRP1 in LysM Cre-expressing cells lead to inadequate adipose vascularization, accelerated weight gain and reduced insulin sensitivity even independent of weight gain. Transfer of NRP1+ hematopoietic cells improved glucose homeostasis, resulting in the reversal of a prediabetic phenotype. Our findings suggest a pivotal role for adipose tissue resident NRP1+-expressing macrophages in driving healthy weight gain and maintaining glucose tolerance.
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Project description:Transcriptional profiling of mouse bone marrow derived macrophages comparing wildtype with CDK5R1 knockout. CDK5R1 is an activating parter for CDK5 and synthesized upon TLRs stimaultion. Activated CDK5 has various target substrates, and functions as a key singnaling regulator in macrophages. Two condition experiments: basal state and LPS-stimulated macrophages for 6 hours. Two biological replicates.
2014-11-20 | E-GEOD-63443 | biostudies-arrayexpress
Project description:Transcriptional profiling of mouse bone marrow derived macrophages comparing wildtype with CDK5R1 knockout. CDK5R1 is an activating parter for CDK5 and synthesized upon TLRs stimaultion. Activated CDK5 has various target substrates, and functions as a key singnaling regulator in macrophages.
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Project description:We report here the deep sequencing of the mRNA from peritoneal exudate cells (macrophages) purified from wildtype or Ptpn1 (PTP1B) knockout mice, either treated or untreated with IL-10. In periotenal macrophages IL-10 activates the transcription factor STAT3 to execute and anti-inflammatory gene expression programme. The tyrosine phosphatase PTPN1 targets STAT3 for dephosphorylation and leads to the deactivation of STAT3. In this study we examined the role of PTP1B in controlling the normal homeostatic level phosphorylation of STAT3 by comparing the IL-10/STAT3-mediated anti-inflammatory gene expression programme. We find that loss of PTP1B leads to an up-regulation of the activity of STAT3, both at the level of phosphorylation and also in enhanced expression of anti-inflammatory gene products. RNA-seq of wildtype and Ptpn1 (PTP1B) knockout mouse peritoneal macrophages, treated or untreated with IL-10
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Project description:To compare subpopulations of Treg cells in wild type mice based upon Nrp1 Expression, differentiating nTreg and iTreg Cells were FACS sorted based upon expression of CD4, Foxp3 and expression of Nrp1.
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Project description:Nrf2 Knockout vs. Wildtype mice
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Project description:Compared to wildtype macrophages, IRAK2 deficient macrophages show higher induced gene expression in responsse to CpG B, but not R848 Manuscipt title: The dual function of IRAK2 in TLR9-mediated interfereon and proinflammatory cytokine production Bone marrow derived macrophages from wildtype and IRAK2 knockout mouse were stimulated with CpG B or R848 for 2 hours, or untreated.
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Project description:To compare subpopulations of Treg cells in wild type mice based upon Nrp1 Expression, differentiating nTreg and iTreg
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Project description:In situ synthesized oligo arrays, U74Av2, from Affymetrix were used to measure differential gene expression in RNA samples generated from the liver of Nrf2 knockout and wildtype mice at 5 month age. Total RNAs from two Nrf2 knockout or wildtype littermates were analyzed separately. There are two replicates (GSM 13431, 13435) for the female Nrf2 wildtype group, two replicates (GSM 13439, 13441) for the male Nrf2 wildtype group, two replicates (GSM 13436, 13437) for the female Nrf2 knockout group, and two replicates (GSM 13438, 13440) for the male Nrf2 knockout group. Keywords: parallel sample
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Project description:Neuropilin-1 (NRP1), a co-receptor for various cytokines, including TGF-β, has been identified as a potential therapeutic target for fibrosis. However, its role and mechanism in renal fibrosis remains elusive. Here, we show that NRP1 is upregulated in distal tubular (DT) cells of patients with transplant renal insufficiency and mice with renal ischemia-reperfusion (I-R) injury. Knockout of Nrp1 reduced multiple endpoints of renal injury and fibrosis. We found that Nrp1 facilitates the binding of TNF-α to its receptor in DT cells after renal injury. This signaling results in a downregulation of lysine crotonylation of the metabolic enzyme Cox4i1, decreased cellular energetics and exacerbation of renal injury. Furthermore, by single-cell RNA-sequencing we found that Nrp1-positive DT cells secrete collagen and communicate with myofibroblasts, exacerbating acute kidney injury (AKI)-induced renal fibrosis by activating Smad3. Dual genetic deletion of Nrp1 and Tgfbr1 in DT cells better improves renal injury and fibrosis than either single knockout. Together, these results reveal that targeting of NRP1 represents a promising strategy for the treatment of AKI and subsequent chronic kidney disease.
2024-06-03 | PXD052293 | Pride