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Effects of Pd1 targeted myeloid deletion on brain development

ABSTRACT: During early brain development, the nervous system continues to evolve and improve, and cells in different stages contact and connect to form a unique nervous system network. Various cross-talk between cell populations is the key to neurological homeostasis. Communication between astrocytes and myeloid cells affects brain function. Programmed cell death protein 1 (PDCD1), also known as PD-1 or CD279 (differentiation cluster 279), is a member of the immunoglobulin gene superfamily. Here, we investigated the loss of PD-1 in myeloid cells results in abnormal development of the nervous system. Specific ablation of PD-1 affects myeloid cell proliferation and subtype classification. At the stage of astrogenesis onset, the astrocyte proliferation ends, and the continuous development, the results of immunofluorescence staining with different astrocyte markers show that astrocytes-related genes were highly expressed in PD-1f/flysMCre mice. PD-1f/flysMCre mice exhibited more outgoing, less anxious, and a more extroverted mode of exploration in behavioral tests. The specific ablation of PD-1 increases the expression of CXCL1 through the NF-κB signaling pathway. It reaches the brain and interacts with CXCR2 on astrocytes, promoting astrocyte proliferation. Our results not only reveal an important regulatory role of PD-1 in myeloid cells on astrocytes but also provide some theoretical basis and ideas for the study of myeloid and brain axis

ORGANISM(S): Mus musculus

PROVIDER: GSE277873 | GEO | 2024/09/30

REPOSITORIES: GEO

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Project description:MartínJiménez2017 - Genome-scale reconstruction of the human astrocyte metabolic network This model is described in the article: Genome-Scale Reconstruction of the Human Astrocyte Metabolic Network. Martín-Jiménez CA, Salazar-Barreto D, Barreto GE, González J. Front Aging Neurosci 2017; 9: 23 Abstract: Astrocytes are the most abundant cells of the central nervous system; they have a predominant role in maintaining brain metabolism. In this sense, abnormal metabolic states have been found in different neuropathological diseases. Determination of metabolic states of astrocytes is difficult to model using current experimental approaches given the high number of reactions and metabolites present. Thus, genome-scale metabolic networks derived from transcriptomic data can be used as a framework to elucidate how astrocytes modulate human brain metabolic states during normal conditions and in neurodegenerative diseases. We performed a Genome-Scale Reconstruction of the Human Astrocyte Metabolic Network with the purpose of elucidating a significant portion of the metabolic map of the astrocyte. This is the first global high-quality, manually curated metabolic reconstruction network of a human astrocyte. It includes 5,007 metabolites and 5,659 reactions distributed among 8 cell compartments, (extracellular, cytoplasm, mitochondria, endoplasmic reticle, Golgi apparatus, lysosome, peroxisome and nucleus). Using the reconstructed network, the metabolic capabilities of human astrocytes were calculated and compared both in normal and ischemic conditions. We identified reactions activated in these two states, which can be useful for understanding the astrocytic pathways that are affected during brain disease. Additionally, we also showed that the obtained flux distributions in the model, are in accordance with literature-based findings. Up to date, this is the most complete representation of the human astrocyte in terms of inclusion of genes, proteins, reactions and metabolic pathways, being a useful guide for in-silico analysis of several metabolic behaviors of the astrocyte during normal and pathologic states. This model is hosted on BioModels Database and identified by: MODEL1608180000. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Effects of Pd1 targeted myeloid deletion on brain development

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