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Genome-wide analysis of microRNA-22 responsive gene expression in lung antigen presenting cells in response to chronic nanoparticulate carbon black exposure

ABSTRACT: Analysis of lung CD11c+ antigen presenting cells (APCs) isolated from wildtype or Mir22-/- mice exposed to nanoparticulate carbon black (nCB) for one month. MiR-22 plays important roles in nCB induced experimental emphysema through regulating APC activation. Results provide insight into the biological role and target genes of miR-22. Smoking-related emphysema is a chronic inflammatory disease driven by T helper 17 (TH17) cells through molecular mechanisms that remain obscure. Here we have explored the role of microRNA-22 (miR-22) in emphysema. MiR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism involving NF-kappaB. MiR-22-deficient mice, but not wild-type, showed attenuated TH17 responses and failed to develop emphysema after exposure to either smoke or nCB. We further show that miR-22 controls APC activation and TH17 responses through activation of AP-1 transcription factor complexes and histone deacetylase (HDAC) 4. Thus, miR-22 is a critical regulator of both emphysema and TH17 responses.

ORGANISM(S): Mus musculus

PROVIDER: GSE72734 | GEO | 2015/09/05

SECONDARY ACCESSION(S): PRJNA294843

REPOSITORIES: GEO

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Genome-wide analysis of microRNA-22 responsive gene expression in lung antigen presenting cells in response to chronic nanoparticulate carbon black exposure

Project description:Analysis of lung CD11c+ antigen presenting cells (APCs) isolated from wildtype or Mir22-/- mice exposed to nanoparticulate carbon black (nCB) for one month. MiR-22 plays important roles in nCB induced experimental emphysema through regulating APC activation. Results provide insight into the biological role and target genes of miR-22. Smoking-related emphysema is a chronic inflammatory disease driven by T helper 17 (TH17) cells through molecular mechanisms that remain obscure. Here we have explored the role of microRNA-22 (miR-22) in emphysema. MiR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism involving NF-kappaB. MiR-22-deficient mice, but not wild-type, showed attenuated TH17 responses and failed to develop emphysema after exposure to either smoke or nCB. We further show that miR-22 controls APC activation and TH17 responses through activation of AP-1 transcription factor complexes and histone deacetylase (HDAC) 4. Thus, miR-22 is a critical regulator of both emphysema and TH17 responses. Lung APCs were isolated from PBS (reference groups) or nCB exposed wildtype or Mir22-/- mice, total four groups. There were three replicates in each group.

2015-09-05 | E-GEOD-72734 | biostudies-arrayexpress

The microRNA miR-22 represses T helper 17 cell pathogenicity by targeting PTEN-regulated pathways

Project description:Multiple sclerosis is a chronic autoimmune disease driven by pathogenic Th17 cells. Here, we dissected the role of miR-22 in pathogenic Th17 cells by autoantigen-specific disease models. We first showed that miR-22 was upregulated in peripheral lymphoid organs and spinal cords of mice developed autoimmune encephalomyelitis. Although miR-22 was upregulated in multiple helper T cell subsets, it was dispensable for T helper cell differentiation in vitro. While miR-22-/- mice exhibited milder symptoms of disease in an active EAE model, adoptive transfer of miR-22-/- 2D2 Th17 cells into naive recipient mice promoted higher disease incidence and severity compared to mice transferred with control 2D2 Th17 cells. Global transcriptional analysis of miR-22-deficient pathogenic Th17 cells revealed upregulated genes in phosphatase and tensin homologue (PTEN)-mediated pathways, and Pten was further identified as one of its potential targets. Therefore, we identified that Th17 cell intrinsic-miR-22 could protect mice from autoimmunity by targeting PTEN-regulated pathways.

2020-05-22 | GSE134895 | GEO

Adipocyte Precursor Cells from First Degree Relatives of type 2 diabetic patients feature changes of hsa-mir-23a-5p, -193a-5p, and -193b-5p and Insulin-Like Growth Factor 2 expression [smallRNA-seq]

Project description:First-degree relatives (FDRs) of type 2 diabetics (T2D) feature dysfunction of subcutaneous adipose tissue (SAT) long before T2D onset. miRNAs have a role in adipocyte precursor cells (APC) differentiation and in adipocyte identity. Thus, impaired miRNA expression may contribute to SAT dysfunction in FDRs. In the present work, we have explored changes of miRNA expression associated with T2D family history which may affect gene expression in SAT APCs from FDRs. Small RNA-seq was performed in APCs from healthy FDRs and matched controls and omics data were validated by qPCR. Integrative analyses of APC miRNome and transcriptome from FDRs revealed down-regulated hsa-miR-23a-5p, -193a-5p and -193b-5p accompanied by up-regulated Insulin-like Growth Factor 2 (IGF2) gene which proved to be their direct target. The expression changes of these marks were associated with SAT adipocyte hypertrophy in FDRs. APCs from FDRs further demonstrated reduced capability to differentiate into adipocytes. Treatment with IGF2 protein decreased APC adipogenesis, while over-expression of hsa-miR-23a-5p, -193a-5p and -193b-5p enhanced adipogenesis by IGF2 targeting. Indeed, IGF2 increased the Wnt Family Member 10B gene expression in APCs. Down-regulation of the three miRNAs and IGF2 up-regulation were also observed in Peripheral Blood Leukocytes (PBLs) from FDRs. In conclusion, APCs from FDRs feature a specific miRNA/gene profile, which associates with SAT adipocyte hypertrophy and appears to contribute to impaired adipogenesis. PBL detection of this profile may help in identifying adipocyte hypertrophy in individuals at high risk of T2D.

2021-11-19 | GSE162133 | GEO

Adipocyte Precursor Cells from First Degree Relatives of type 2 diabetic patients feature changes of hsa-mir-23a-5p, -193a-5p, and -193b-5p and Insulin-Like Growth Factor 2 expression [RNA-Seq]

2021-11-19 | GSE161989 | GEO

Genome-wide analysis of lung myeloid dendritic cells gene expression from healthy or emphysema subjects

Project description:Lung myeloid dendritic cells isolated from emphysema but not healthy subjects induce Th1 and Th17 cells differentiation. The goal of this study is to identify the genes differentially expressed by lung myeloid dendritic cells from healthy or emphysema subjects. These genes may play crucial roles in directing Th1 and Th17 cells differentiation. Total mRNA was extracted from lung myeloid dendritic cells isolated from lungs of three healthy controls and three emphysema patients.

2011-01-01 | E-GEOD-26296 | biostudies-arrayexpress

Fibroblast growth factor (FGF) 10 is essential for lung morphogenesis

Project description:Fibroblast growth factor (FGF) 10 is essential for lung morphogenesis and polymorphisms in the Fgf10 region are linked with higher susceptibility towards COPD in human patients. We found that FGF10 signaling is impaired in lung septal wall compartment from COPD patients. Mice with impaired FGF10 signaling (Fgf10+/-) were more prone to develop cigarette smoke (CS)-induced emphysema and pulmonary hypertension (PH). Furthermore, FGF10 overexpression could successfully reverse cigarette smoke-induced emphysema and PH in mice.

2024-04-01 | GSE230854 | GEO

miR-155 promotes Th17 development by targeting Jarid2

Project description:Genome-wide analysis was performed on microRNA 155+/+ and -/- Th17 cells to determine the differentially expressed transcripts that are regulated by miR-155. We found that Jarid2 was differentially expressed in absence of miR-155 and highlight the mechanism for the silencing of IL-22 by Jarid2 and PRC2 in miR-155-/- Th17 cells.

2014-10-12 | GSE37228 | GEO

Genome-wide analysis of lung myeloid dendritic cells gene expression from healthy or emphysema subjects

2011-01-01 | GSE26296 | GEO

Identification of metabolically distinct adipocyte progenitor cells in human adipose tissues

Project description:Adipocyte progenitor cells (APCs) provide the reservoir of regenerative cells to produce new adipocytes, although their identity in humans remains elusive. Using FACS analysis, gene expression profiling and metabolic and proteomic analyses, we identified three APCs subtypes in human white adipose tissues. The APC subtypes are molecularly distinct but possess similar proliferative and adipogenic capacities. Adipocytes derived from APCs with high CD34 expression exhibit exceedingly high rates of lipid flux compared with APCs with low or no CD34 expression, while adipocytes produced from CD34- APCs display beige-like adipocyte properties and a unique endocrine profile. APCs were more abundant in gluteofemoral compared with abdominal subcutaneous and omental adipose tissues, and the distribution of APC subtypes varies between depots and in patients with type 2 diabetes. These findings provide a mechanistic explanation for the heterogeneity of human white adipose tissue and a potential basis for dysregulated adipocyte function in type 2 diabetes.

2019-04-25 | GSE129042 | GEO

mouse lung resistance or sensitivity to cigarette smoke

Project description:We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype.

2008-07-10 | GSE12036 | GEO

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