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Young and aged Myeloid cell treatment with EP2 antagonist PF044

ABSTRACT: Young and aged Myeloid cell treatment with EP2 antagonist PF044

PROVIDER: PRJNA656279 | ENA |

REPOSITORIES: ENA

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Young and aged Myeloid cell treatment with EP2 antagonist PF044

Project description:Peritoneal macrophages from young (3-4mo.) and aged (20-22mo.) mice were isolated from mice treated with EP2 antagonist PF044 (2.5mg/kg/d) for 6 weeks.

2020-11-24 | GSE155992 | GEO

Young and aged mouse bladders

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MCG 101 tumors implanted on prostaglandin receptor EP2 wildtype and EP2 knockout mice

Project description:Wild type tumor cells, producing high levels of prostaglandin E2 (MCG101, EP2 +/+), were inoculated on EP2 knockout (EP2 -/-) and EP2 wild type (EP2 +/+) mice. Solid tumors were dissected into tumor- and tumor-stroma tissue compartments for RNA expression microarray screening, followed by metabolic pathway analyses. The study aims to evaluate simultaneous gene pathway expressions in separate tissue compartments, such as isolated tumor tissue and tumor stroma respectively.

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Inhibition of PGE2-EP2/EP4 signaling elicits anti-tumor immunity through reprograming of inflammatory myeloid cells and suppression of mRegDC-Treg axis

Project description:The discovery of immune checkpoint inhibitor (ICI) has highlighted the clinical importance of immune evasion in cancer. However, only a fraction of cancer patients show response to ICI, raising a question on immune suppression mechanisms other than immune checkpoint. In this study, we examined the role of the lipid inflammatory mediator PGE2 in immune evasion of the ICI-insensitive Lewis Lung Carcinoma line 1 (LLC1) mouse model. Inhibition of PGE receptors, EP2 and EP4, significantly suppressed tumor growth through the modulation of host immune cells. Single cell RNA-sequencing analysis revealed that EP2/4 inhibition elicited anti-tumor immunity through the reprogramming of inflammatory myeloid cells by downregulating expression of genes in NFB signaling and actions and suppression of the mregDC-regulatory T cell axis by downregulating genes associated with regulatory T cell recruitment and activation. Taken together, our work suggests that PGE2-EP2/EP4 signaling induces proinflammatory myeloid and tolerogenic lymphoid environments in ICI-insensitive tumors, which is amenable to EP2 and EP4 inhibitors..

2022-06-14 | GSE169688 | GEO

scRNAseq of spleen and atherosclerotic plaques from young and aged healthy and young and aged atherosclerotic mice

Project description:T cells change substantially with age and are involved in atherosclerosis. Aging is the strongest clinical risk factor for atherosclerosis so we profiled T cells in young and aged mice prior to atherosclerosis (healthy) and in young and aged atherosclerotic mice (diseased).

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Aged, Young and Restored Samples from Mobilized Peripheral Blood [mRNA]

Project description:We report the gene expression changes in mobilized peripheral blood in aged, young, and aged/young samples cocultured in transwell. Restored samples refer to aged MPB co-cultured with young MPB in the transwell culture

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sperm proteome of aged and young males

Project description:we build the sperm proteome profile of aged and young males

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Single cell RNA sequencing of myeloid cells from lungs of young and aged mice

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Aged, Young and Restored Samples from Mobilized Peripheral Blood [miRNA]

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Differentiation of young and replicatively aged mouse C2C12 muscle cells

Project description:Age-related impairments in myoblast differentiation may contribute to reductions in muscle function in older adults but the underlying proteostasis processes are not well understood. We investigated young (P6-10) and replicatively aged (P48-50) C2C12 myoblast cultures during early (0h-24h) and late (72h-96h) stages of differentiation using deuterium oxide (D2O) labelling and mass spectrometry. The absolute dynamic profiling technique for proteomics (Proteo-ADPT) was used to quantify the absolute rates of abundance change, synthesis and degradation of individual proteins. Proteo-ADPT encompassed 116 proteins and 74 proteins exhibited significantly (P<0.05, FDR <5 %) different changes in abundance between young and aged cells at early and later periods of differentiation. Young cells exhibited a steady pattern of growth, protein accretion and fusion, whereas aged cells failed to gain protein mass or undergo fusion during later differentiation. Maturation of the proteome was retarded in aged myoblasts at the onset of differentiation, but the proteome appeared to ‘catch up’ with the young cells during the early differentiation period. However, this ‘catch up’ process in aged cells was not accomplished by higher levels of protein synthesis. Instead, a lower level of protein degradation in aged cells was responsible for the elevated gains in protein abundance. Our novel data point to a loss of proteome quality as a precursor to the lack of fusion of aged myoblasts and highlights dysregulation of protein degradation, particularly of ribosomal and chaperone proteins, as a key mechanism that may contribute to age-related declines in the capacity of myoblasts to undergo differentiation.

2023-06-27 | PXD029515 | Pride

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