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Ptdsr-/- (phosphatidylserine receptor) fibroblasts

ABSTRACT: Phagocytosis of apoptotic cells is fundamental to animal development, immune function and cellular homeostasis. The phosphatidylserine receptor (Ptdsr) on phagocytes has been implicated in the recognition and engulfment of apoptotic cells and in anti-inflammatory signaling. Ptdsr is essential for the development and differentiation of multiple organs during embryogenesis. Ptdsr may thus have a novel, unexpected developmental function as an important differentiation-promoting gene. Moreover, Ptdsr is not required for apoptotic cell clearance by macrophages but seems to be necessary for the regulation of macrophage cytokine responses. Keywords: ptdsr, fibroblast, cDNA microarray experiments,

ORGANISM(S): Mus musculus

PROVIDER: GSE6937 | GEO | 2007/03/01

SECONDARY ACCESSION(S): PRJNA98115

REPOSITORIES: GEO

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Ptdsr (phosphatidylserine receptor) embryos

Project description:Phagocytosis of apoptotic cells is fundamental to animal development, immune function and cellular homeostasis. The phosphatidylserine receptor (Ptdsr) on phagocytes has been implicated in the recognition and engulfment of apoptotic cells and in anti-inflammatory signaling. Ptdsr is essential for the development and differentiation of multiple organs during embryogenesis but not for apoptotic cell removal. Ptdsr may thus have a novel, unexpected developmental function as an important differentiation-promoting gene. Moreover, Ptdsr is not required for apoptotic cell clearance by macrophages but seems to be necessary for the regulation of macrophage cytokine responses. Keywords: ptdsr, embryo E11.5, E12.5, E13.5, cDNA microarray experiments

2007-03-01 | GSE6938 | GEO

Gene expression profiles in Drosophila phagocytes after incubation with apototic cell fragments

Project description:The phagocytic elimination of cells undergoing apoptosis is an evolutionarily conserved innate immune mechanism for eliminating unnecessary cells. Previous studies showed an increase in the level of engulfment receptors in phagocytes after the phagocytosis of apoptotic cells, which leads to the enhancement of their phagocytic activity. However, precise mechanisms underlying this phenomenon require further clarification. We found that the pre-incubation of a Drosophila phagocyte cell line with the fragments of apoptotic cells enhanced the subsequent phagocytosis of apoptotic cells, accompanied by an augmented expression of the engulfment receptors Draper and integrin αPS3. The DNA-binding activity of the transcription repressor Tailless was transiently raised in those phagocytes, depending on two partially overlapping signal-transduction pathways for the induction of phagocytosis as well as the occurrence of engulfment. The RNAi knockdown of tailless in phagocytes abrogated the enhancement of both phagocytosis and engulfment receptor expression. Furthermore, the hemocyte-specific RNAi of tailless reduced apoptotic cell clearance in Drosophila embryos. Taken together, we propose the following mechanism for the activation of Drosophila phagocytes after an encounter with apoptotic cells: two partially overlapping signaltransduction pathways for phagocytosis are initiated; transcription repressor Tailless is activated; expression of engulfment receptors is stimulated; and phagocytic activity is enhanced. This phenomenon most likely ensures the phagocytic elimination of apoptotic cells that stimulated phagocytes find thereafter and is thus considered as a mechanism to prime phagocytes in innate immunity.

2017-03-23 | GSE85429 | GEO

Macrophages redirect phagocytosis by non-professional phagocytes and influence inflammation

Project description:Professional phagocytes (such as macrophages) and non-professional phagocytes (such as epithelial cells) clear billions of apoptotic cells and particles on a daily basis. Since these phagocytes reside in proximity in most tissues, whether cross-communication exists between them during cell clearance, and how this might impact inflammation are not known. Here, we show that macrophages, via the release of a soluble growth factor and microvesicles, redirect the type of particles engulfed by non-professional phagocytes and influence their inflammatory response. During apoptotic cell engulfment or in response to inflammation-associated cytokines, macrophages released insulin-like growth factor 1 (IGF-1). The binding of IGF-1 to its receptor on non-professional phagocytes redirected their phagocytosis, such that uptake of larger apoptotic cells was dampened while engulfment of microvesicles was enhanced. Macrophages were refractory to this IGF-1 mediated engulfment modulation. Macrophages also released microvesicles, whose uptake by epithelial cells, enhanced by IGF-1, led to decreased inflammatory responses by epithelial cells. Consistent with these observations, deletion of IGF-1 receptor in airway epithelial cells led to exacerbated lung inflammation after allergen exposure. These genetic and functional studies reveal a novel IGF-1 and microvesicle-dependent communication between macrophages and epithelial cells that can critically influence the magnitude of tissue inflammation in vivo.

2016-11-01 | GSE89049 | GEO

Expression data from intestinal dendritic cells and macrophages of VDTR mice at 4 hours post diphtheria toxin administration

Project description:Recognition and removal of apoptotic cells by professional phagocytes, including dendritic cells and macrophages, preserve self-tolerance and prevent chronic inflammation and autoimmune pathologies. However the diverse array of phagocytes residing within different tissues combined with the necessarily prompt nature of apoptotic cell clearance has made it difficult to study this process in situ. Thus, the full spectrum of functions executed by tissue resident phagocytes in response to homeostatic apoptosis remains unclear. We used microarrays to characterize the transcriptome within murine intestinal dendritic cells and macrophages both before and after in situ phagocytosis of apoptotic intestinal epithelial cells.

2016-11-10 | GSE85682 | GEO

Neuronal integrity, not activity, drives synaptic material clearance by microglia after CNS injury

Project description:Phagocytosis of synaptic debris by microglia is critical for CNS development and homeostasis. Less well understood are microglial functions in injured adult brain, where their presumed role is clearance of neuronal debris. Assay of this process is challenging, because the resulting peripheral myeloid-cell engraftment is difficult to dissociate from microglial clearance. The model used here, optic nerve crush injury in adult mouse, stimulates rapid engulfment of synaptic material by microglia residing in the lateral geniculate nucleus (LGN), sufficiently distant from the injury to preclude peripheral-cell engraftment. Pre-injury pharmacological depletion of microglia causes post-injury accumulation of synaptic debris, suggesting that these, not astrocytes, are the dominant post-injury phagocytes. Genetic and pharmacological manipulations revealed that neuronal activity, which regulates microglial engulfment of synaptic debris in development, does not do so in post-injury synaptic material clearance in adulthood, where such clearance depends instead on axonal integrity. RNAseq reveals C1q involvement in clearance of debris by LGN-resident microglia, supporting our finding of its impaired clearance in C1qa-/- and Itgam-/- mice. Our results demonstrate how neurodegenerative debris is cleared by microglial phagocytosis, and offer a model for assaying microglial phagocytic activity and studying its mechanisms and physiological roles.

2018-06-07 | GSE107635 | GEO

Efferocytosis induces a novel SLC program to promote glucose uptake and lactate release

Project description:On a daily basis, we turnover billions of apoptotic cells that are removed by professional and non-professional phagocytes1-10. While characterizing the transcriptional program of phagocytes, we discovered a novel solute carrier family (SLC) gene signature (33 SLC members) that is specifically modified during engulfment of apoptotic cells (efferocytosis) but not during antibody-mediated phagocytosis. When we assessed the functional relevance of these SLCs, we noted robust induction of an aerobic glycolysis program in engulfing phagocytes, initiated by SLC2A1-mediated glucose uptake, and suppression of oxidative phosphorylation program. Interestingly, the different steps of phagocytosis10,11, i.e. smell (‘find-me’ signals / sensing factors released by apoptotic cells), taste (phagocyte- apoptotic cell contact), and ingestion (corpse internalization), activated different molecules to promote this glycolytic process. Further, lactate, a natural by-product of aerobic glycolysis12,13, was released from engulfing phagocytes via SLC16A1, an SLC member activated after corpse uptake. While glycolysis within phagocytes contributed to actin polymerization and the continued uptake of corpses, the lactate released via SLC16A1 influenced the establishment of an anti-inflammatory environment. Collectively, these data reveal a novel SLC program activated during efferocytosis, identify a previously unknown reliance on aerobic glycolysis during apoptotic cell uptake, and that glycolytic byproducts of efferocytosis can also influence other cells in the microenvironment.

2018-11-30 | GSE119273 | GEO

MiR-471-5p–Dependent Regulation of Phagocytosis/Autophagy-Associated Proteins

Project description:Phagocytic clearance of apoptotic germ cells by Sertoli cells is vital for germ cell development and differentiation. Using a tissue-specific miRNA transgenic mouse model, we show that interaction between miR-471-5p and autophagy member proteins regulates clearance of apoptotic germ cells via LC3-associated phagocytosis (LAP).

2017-11-01 | GSE99500 | GEO

Jedi-1/MEGF12-mediated phagocytosis controls the pro-neurogenic properties of microglia in the ventricular-subventricular zone

Project description:Microglia are the primary phagocytes in the central nervous system and are responsible for clearing dead cells generated during development or disease. The phagocytic process shapes the phenotype of the microglia, which affects the local environment. A unique population of microglia reside in the ventricular-subventricular zone (V-SVZ) of neonatal mice, but how they influence this neurogenic niche is not well-understood. Here, we demonstrate that phagocytosis creates a pro-neurogenic microglial phenotype in the V-SVZ and that these microglia phagocytose apoptotic cells via the engulfment receptor Jedi-1. Deletion of Jedi-1 decreases apoptotic cell clearance, triggering the development of a neuroinflammatory phenotype, reminiscent of neurodegenerative and-age-associated microglia, that reduces neural precursor proliferation via elevated interleukin (IL)-1β signaling; inhibiton of IL-1 receptor rescues precursor proliferation in vivo. Together, these results reveal a critical role for Jedi-1 in connecting microglial phagocytic activity to a phenotype that promotes neurogenesis in the developing V-SVZ. We performed RNAseq on MACS-sorted microglia from V-SVZ and Cortex of WT and Jedi-1 knockout P7 mice.

2024-02-15 | GSE232441 | GEO

C. elegans DYN-1 interacting proteins

Project description:We found that NDK-1/NDPK functions together with DYN-1/Dynamin to trigger membrane remodeling events during apoptotic cell clearance, including engulfment and phagosome maturation. We showed by IP-Mass Spec studies that C. elegans NDK-1/NDPK and DYN-1/Dynamin function in the same complex.

2017-12-27 | MSV000081868 | MassIVE

Tafazzin Regulates Cell State by Modulating Phosphatidylethanolamine and Phosphatidylserine levels

Project description:Inhibiting tafazzin a cardiolipin remodeling enzyme reduces stemness of AML by modulating the level of phosphatidylserine

2019-03-28 | GSE107045 | GEO