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Gene expression profiles of the lung of CD2-T-bet transgenic mice

ABSTRACT: To uncover potential mechanisms underlying the observed Pulmonary Alveolar Proteinosis-like phenotype, we performed a microarray analysis using lung mRNAs from T-bet transgenic mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE62637 | GEO | 2014/11/03

SECONDARY ACCESSION(S): PRJNA264610

REPOSITORIES: GEO

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Gene expression profiles of the lung of CD2-T-bet transgenic mice

Project description:To uncover potential mechanisms underlying the observed Pulmonary Alveolar Proteinosis-like phenotype, we performed a microarray analysis using lung mRNAs from T-bet transgenic mice. Gene expression signatures associated with pulmonary alveolar proteinosis induced by T-bet overexpression in T cells were measured.

2014-11-03 | E-GEOD-62637 | biostudies-arrayexpress

Expression profiles and potential functions of long non-coding RNAs and mRNAs in autoimmune pulmonary alveolar proteinosis patients

Project description:Autoimmune pulmonary alveolar proteinosis (APAP) is a rare lung disease which may be closely associated with autoantibody. However, there is little known about the function of long non-coding RNAs (lncRNAs) in APAP.To further investigate the role of lncRNAs in APAP, we screened the differential expression profiles of lncRNAs and mRNAs in peripheral blood samples between five APAP patients and five matched healthy controls. We analyzed the regulatory networks of lncRNA-mRNA and lncRNA-miRNA-mRNA via bioinformatics methods. This study identified differentially expressed (DE) lncRNAs and their potential corresponding mRNAs to provide a basis for the study of APAP pathogenesis.

2021-04-28 | GSE153957 | GEO

Project description:GM-CSF receptor-Î² deficient (Csf2rbâ/â or KO) mice develop a lung disease identical to hereditary pulmonary alveolar proteinosis (hPAP) in humans with recessive CSF2RA or CSF2RB mutations that impair GM-CSF receptor function. We performed pulmonary macrophage transplantation (PMT) of bone marrow derived macrophages (BMDMs) without myeloablation in Csf2rbâ/âmice. BMDMs were administered by endotracheal instillation into 2 month-old Csf2rbâ/â mice. Results demonstrated that PMT therapeutic of hPAP in Csf2rbâ/â mice was highly efficacious and durable. Alveolar macrophages were isolated by bronchoalveolar lavage one year after administration subjected to microarray analysis to determine the effects of PMT therapy on the global gene expression profile. Total mRNA was isolated from alveolar macrophages PMT-treated Csf2rbâ/âmice (PMT) and from age-matched, untreated KO mice (KO) and wild-type (C57Bl/6) mice (WT). Total mRNA was evaluated using Affymetrix microarrays (Mouse Gene 1.0 ST Array) to compare the gene expression profiles among the three groups (3 mice/group).

2014-10-01 | E-GEOD-60528 | biostudies-arrayexpress

Expression profiles and potential functions of long non-coding RNAs and mRNAs in autoimmune pulmonary alveolar proteinosis patients

Project description:Expression profiles and potential functions of long non-coding RNAs and mRNAs in autoimmune pulmonary alveolar proteinosis patients

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Project description:GM-CSF receptor-β deficient (Csf2rb–/– or KO) mice develop a lung disease identical to hereditary pulmonary alveolar proteinosis (hPAP) in humans with recessive CSF2RA or CSF2RB mutations that impair GM-CSF receptor function. We performed pulmonary macrophage transplantation (PMT) of bone marrow derived macrophages (BMDMs) without myeloablation in Csf2rb–/–mice. BMDMs were administered by endotracheal instillation into 2 month-old Csf2rb–/– mice. Results demonstrated that PMT therapeutic of hPAP in Csf2rb–/– mice was highly efficacious and durable. Alveolar macrophages were isolated by bronchoalveolar lavage one year after administration subjected to microarray analysis to determine the effects of PMT therapy on the global gene expression profile.

2014-10-01 | GSE60528 | GEO

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Project description:Tissue resident macrophages show their specific function to maintain homeostasis in our body. Dysfunction of alveolar macrophages (AMs), which regulate the proper amount of surfactant protein, leads to the development of pulmonary alveolar proteinosis (PAP). Here we found that inflammation ruins the function of AMs and is one of the causes of secondary PAP. Inflammation leads to the loss of specific gene expression pattern of AMs and furthermore, it leads to gain the specific gene expression pattern of other tissue resident macrophages and DC lineage. We also found the critical roles for Bach2 expressed in AMs and T cells, whose expression is induced by IFNg released from T cells. Bach2 bounds to super-enhancer regions of the inflammatory genes of the myeloid lineage and represses excess inflammation in lungs. Our results suggest that Bach2 function among several cell lineages to modify the inflammation, maintaining homeostasis in lungs.

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Project description:Pulmonary alveolar proteinosis (PAP) is a syndrome characterized by accumulation of surfactant lipoproteins within the lung alveoli. Alveolar macrophages (AMs) are crucial for surfactant clearance and their differentiation depends on colony-stimulating factor 2 (CSF2) and the establishment of an AM-characteristic gene regulatory network. Here we report that the transcription factor C/EBPβ is essential for the development of the AM identity, as demonstrated by transcriptome and chromatin accessibility analysis. Furthermore, C/EBPβ-deficient AMs showed severe defects in proliferation, phagocytosis and lipid metabolism, collectively resulting in a PAP-like syndrome. Mechanistically, the long C/EBPβ protein variants LAP* and LAP together with CSF2 signaling induced expression of Pparg isoform2, but not isoform1, a molecular regulation that was also observed in other CSF2-primed macrophages. These results uncover C/EBPβ as a key regulator of AM cell fate and as the missing link between CSF2 and Pparg isoform 2 expression, thereby regulating lipid turnover in AMs.

2022-09-16 | GSE173970 | GEO

Multicenter International Retrospective Cross-sectional Evaluation of Pulmonary Alveolar Proteinosis (MICEPAP) Trial - RLD 5706

Project description:Multicenter International Retrospective Cross-sectional Evaluation of Pulmonary Alveolar Proteinosis (MICEPAP) Trial - RLD 5706

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Homo sapiens

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