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ATAC-seq to profile the chromatin accessibility in WT and Phlpp1-deficient BMDMs

ABSTRACT: To identify chromatic alterations by Phlpp1 deficiency in BMDMs, we performed ATAC-sequencing. We identified regions of chromatin that were altered in Phlpp1 deficiency BMDMs after exposure to IL-4 for 4 h.

ORGANISM(S): Mus musculus

PROVIDER: GSE252726 | GEO | 2025/12/31

REPOSITORIES: GEO

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ATAC-seq to profile the chromatin accessibility in WT and Phlpp1-deficient BMDMs

Project description:ATAC-seq to profile the chromatin accessibility in WT and Phlpp1-deficient BMDMs

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Next Generation Sequencing Facilitates Quantitative Analysis of wild type and Phlpp1-deficient Bone Marrow Derived macrophage Transcriptomes

Project description:Purpose: The purpose of this study is to detect activated or silenced genes during wild type (WT) and Phlpp1-deficient bone marrow derived macrophages (BMDMs). Gene expression differences between two samples could be found using transcriptome profiling (RNA-seq) analysis. Methods: Mouse BMDMs were generated from bone marrow cells in RPMI-1640 medium with recombinant mouse M-CSF (20ng/ml). BMDMs were stained to confirm the surface expression of CD11b and F4/80. Cells with purity >97.5% were used for subsequent experiments. WT and Phlpp1 deficient BMDMs were stimulated with IL-4 (20ng/ml) for 12 and 24 hours, of which RNA profiles were generated by deep sequencing, using Illumina. Results: We mapped about 10 million sequence reads per sample to the mouse genome, identified hundreds of genes with significant mRNA between WT and Phlpp1 deficient BMDMs.

2025-12-31 | GSE252728 | GEO

PHLPP1 Cut&Tag profiling of bone marrow derived macrophage

Project description:Purpose: To transcriptome widely reveal genes regulation by PHLPP1, we performed Cleavage Under Targets and Tagmentation (CUT&Tag) analysis of wild-type (WT) BMDMs. Methods: Mouse BMDMs were generated from bone marrow cells in RPMI-1640 medium with recombinant mouse M-CSF (20ng/ml). BMDMs were stained to confirm the surface expression of CD11b and F4/80. Cells with purity >97.5% were used for subsequent experiments. WT BMDMs were stimulated with IL-4 (20ng/ml) for 4 hours. Results: We carried out a CUT&Tag assay using antibodies against PHLPP1, and found the global influence of PHLPP1 in regulating genes of transcription regulatory regions of key genes for pro-fibrosis macrophage effector function.

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Phlpp1-deficient macrophages

Project description:Phlpp1-deficient macrophages

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Phlpp1 regulates endochondral ossification via the chondrocyte phospho-proteome

Project description:Appendicular growth and bone mass acquisition are controlled by a variety of growth factors, hormones, and mechanical forces in a dynamic process called endochondral ossification. Chondrocytes in the growth plate must proliferate and undergo hypertrophy to drive growth plate expansion and lay the template for bone. Pleckstrin homology (PH) domain and leucine rich repeat phosphatase 1 and 2 (Phlpp1 and Phlpp2) are protein phosphatases that regulate intracellular signaling cascades through posttranslational modification of AKT, PKC, and S6K, among others. Phlpp1 controls chondrocyte proliferation and survival and germline deletion of Phlpp1 suppresses bone lengthening. Here, we demonstrate that Phlpp2 does not regulate endochondral ossification. Phlpp2-/- mice are phenotypically indistinguishable from their wildtype (WT) littermates, with similar bone length, bone mass, and growth plate dynamics. By contrast, Phlpp1/2-/- mice are phenotypically indistinguishable from Phlpp1-/- mice. Deletion of Phlpp1 or Phlpp2 had moderate effects on the chondrocyte transcriptome and proteome compared to WT control cells. By contrast, Phlpp1-/- and Phlpp1/2-/- chondrocytes had significantly altered phospho-proteomes compared to WT and Phlpp2-/- chondrocytes. Data integration via multiomics analysis revealed that RAF-MEK-ERK signaling was altered in cells lacking Phlpp1. In conclusion, these data demonstrate that Phlpp1, but not Phlpp2, regulates endochondral ossification via the chondrocyte phospho-proteome.

2024-09-30 | GSE265773 | GEO

Phlpp1 alters the murine chondrocyte phospho-proteome during endochondral bone formation

Project description:Appendicular skeletal growth and bone mass acquisition are controlled by a variety of growth factors, hormones, and mechanical forces in a dynamic process called endochondral ossification. In long bones, chondrocytes in the growth plate proliferate and undergo hypertrophy to drive bone lengthening and mineralization. Pleckstrin homology (PH) domain and leucine rich repeat phosphatase 1 and 2 (Phlpp1 and Phlpp2) are serine/threonine protein phosphatases that regulate cell proliferation, survival, and maturation via Akt, PKC, Raf1, S6k, and other intracellular signaling cascades. Germline deletion of Phlpp1 suppresses bone lengthening in part through parathyroid hormone receptor-dependent signaling in growth plate chondrocytes. Here, we demonstrate that Phlpp2 does not regulate endochondral ossification, and we define the molecular differences between Phlpp1 and Phlpp2 in chondrocytes. Phlpp2-/- mice are phenotypically indistinguishable from their wildtype (WT) littermates, with similar bone length, bone mass, and growth plate dynamics. Deletion of Phlpp2 had moderate effects on the chondrocyte transcriptome and proteome compared to WT cells. By contrast, Phlpp1/2-/- (double knockout) mice resembled Phlpp1-/- mice phenotypically and chondrocyte phospho-proteomes of Phlpp1-/- and Phlpp1/2-/- chondrocytes were different than WT and Phlpp2-/- chondrocyte phospho-proteomes. Data integration via multiparametric analysis identified alterations in Pdpk1 and Pak1/2 signaling pathways in chondrocytes lacking Phlpp1. In conclusion, these data demonstrate that Phlpp1, but not Phlpp2, regulates endochondral ossification through multiple and complex signaling cascades.

2024-10-22 | PXD055563 | Pride

RNA-Seq analysis of WT and Phlpp1-deficient alveolar macrophages in bleomycin-induced PF model

Project description:The purpose of this study is to detect differentially expressed genes in wild-type (WT) and Phlpp1-deficient alveolar macrophages (AMs) 7 days after bleomycin. We performed gene expression profiling of AMs of broncho-alveolar lavage fluid (BALF) from mice that were intratracheally instilled with saline or bleomycin. Gene expression differences between the two samples could be found using transcriptome profiling (RNA-seq) analysis. RNA profiles were generated by deep sequencing, using Illumina. AMs were stained to confirm the surface expression of CD11c and Siglesc-F. Cells with purity >98% were used for subsequent experiments. We identified several differentially expressed genes in the two groups of cells.

2025-12-31 | GSE252727 | GEO

Genome-wide maps of chromatin state and RNA-seq in WT and Dnmt3a KO BMDMs (bone marrow derived macrophages) [RNA-seq]

Project description:To identify soluble factors released from Dnmt3a KO macrophages that might drive differences in osteoclast differentiation, we performed RNA sequencing on unstimulated BMDMs from WT and Dnmt3a KO mice. To investigate the mechanistic basis for the inflammatory phenotype. of myeloid cells with loss of Dnmt3a,we performed reduced representation bisulfite sequencing (RRBS) on Dnmt3a KO and WT BMDMs to assess methylation changes. Concurrently, we performed ATAC-sequencing (ATAC-seq) to assess differences in chromatin accessibility between WT and Dnmt3a KO BMDMs in the context of changes in methylation. We performed chromatin immunoprecipitation sequencing (CHIP-seq) for Irf3 and Rela based on ATAC-seq analysis.

2021-10-07 | GSE183480 | GEO

Genome-wide maps of chromatin state and RNA-seq in WT and Dnmt3a KO BMDMs (bone marrow derived macrophages) [RRBS, ATAC-seq, CHIP-seq]

2021-10-07 | GSE184443 | GEO

Identification of PHLPP1 as a tumor suppressor reveals the role of feedback compensation in PTEN-mutant prostate cancer progression

Project description:Hyper-activation of the PI 3-Kinase/ AKT pathway is a driving force of many cancers. Here we identify the AKT-inactivating phosphatase PHLPP1 as a prostate tumor suppressor. We show that Phlpp1-loss causes neoplasia and, upon partial Pten-loss, carcinoma in mouse prostate. This genetic setting initially triggers a growth suppressive response via p53 and the Phlpp2 ortholog, and reveals spontaneous Trp53 inactivation as a condition for full-blown disease. Surprisingly, the co-deletion of PTEN and PHLPP1 in patient samples is highly restricted to metastatic disease and tightly correlated to deletion of TP53 and PHLPP2. These data establish a conceptual framework for progression of PTEN-mutant prostate cancer to life-threatening disease. To better assess the role of Phlpp in prostate we performed micorarray analysis of gene expression in the WT and Pten+/-; Phlpp1-/- mice.

2011-08-16 | E-GEOD-30987 | biostudies-arrayexpress

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