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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression study of macrophages during early foreign body reaction

ABSTRACT: Foreign body reaction (FBR), initiated by adherence of macrophages to biomaterials, is associated with several complications. Searching for mechanisms potentially useful to overcome these complications, we have established the signaling role of macrophages in the development of FBR. This study profiles gene expression of in vitro fibrinogen activated macrophages as well as that of freshly isolated macrophages from 3-days implants, against a background of unactivated macrophages/monocytes. Total RNA was isolated from fibrinogen activated macrophages, FBR macrophages and macrophages from blood (control). Samples were processed in triplicate on Rat Genome 230 2.0 Array GeneChips, adding up to 9 arrays in total. Microarray processing was performed at DNAVision (Charleroi, Belgium). The RMA comparisons between macrophases are linked below.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Lindsay Mesure

PROVIDER: E-GEOD-21682 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression study of monocytes/macrophages during early foreign body reaction and identification of potential precursors of myofibroblasts.

Mesure Lindsay L De Visscher Geofrey G Vranken Ilse I Lebacq An A Flameng Willem W

PloS one 20100923 9

Foreign body reaction (FBR), initiated by adherence of macrophages to biomaterials, is associated with several complications. Searching for mechanisms potentially useful to overcome these complications, we have established the signaling role of monocytes/macrophages in the development of FBR and the presence of CD34(+) cells that potentially differentiate into myofibroblasts. Therefore, CD68(+) cells were in vitro activated with fibrinogen and also purified from the FBR after 3 days of implantat ...[more]

PMID: 20886081

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Gene expression study of macrophages during early foreign body reaction

Project description:Foreign body reaction (FBR), initiated by adherence of macrophages to biomaterials, is associated with several complications. Searching for mechanisms potentially useful to overcome these complications, we have established the signaling role of macrophages in the development of FBR. This study profiles gene expression of in vitro fibrinogen activated macrophages as well as that of freshly isolated macrophages from 3-days implants, against a background of unactivated macrophages/monocytes.

2013-01-23 | GSE21682 | GEO

Biomaterials direct functional B cell response in a material specific manner

Project description:B cells are an adaptive immune target of biomaterials development in vaccine research but despite their role in wound healing have not been studied tissue engineering and regenerative medicine. We evaluated the B cell response to biomaterial scaffold materials implanted in a muscle wound; a biological extracellular matrix (ECM) and synthetic polyester polycaprolactone. In the local muscle tissue, small numbers of B cells are recruited in response to tissue injury and biomaterial implantation. ECM materials induced plasmablasts in lymph nodes and antigen presentation in the spleen while the synthetic PCL implants delayed B cell migration and induced an antigen presenting phenotype. In muMt- mice lacking B cells, the fibrotic response to the synthetic biomaterials decreased. Immunofluorescence confirmed antigen presenting B cells in fibrotic tissue surrounding silicone breast implants. In sum, the adaptive B cell immune response to biomaterial depends on composition and induces local, regional and systemic immunological changes.

2021-12-01 | GSE182633 | GEO

mRNA gene expression profile analysis in the CD4+ T cells with miR-7 deficiency

Project description:To detect the mRNA gene expression profile in the unactivated and activated CD4+ T cells with miR-7 deficiency.

2021-06-27 | GSE116689 | GEO

Homo sapiens

Project description:Expression data from unactivated vs. activated PBMCs

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Transgenic NUP98-HOXA9 Zebrafish Embryos: Unactivated ('lGl') vs. Cre-activated ('NHA9')

Project description:Transcriptional profiling of zebrafish embryos at 28 hours post fertilization, comparing control 'unactivated' Tg(spi1::lox-eGFP-lox::NHA9) embryos with experimental 'Cre-activated' Tg(spi1::NHA9) embryos. Goal was to determine the effects of expressing NUP98-HOXA9 oncogene on global and blood cell-specific gene expression in early zebrafish development. Two-condition experiment, unactivated 'lGl' embryos vs. Cre-activated 'NHA9' embryos. Biological replicates: 2 control replicates, 2 experimental replicates.

2014-10-30 | E-GEOD-62793 | biostudies-arrayexpress

Single-cell Analysis of Surface Topography-induced Foreign Body Response to Silicone Implants

Project description:Silicone-based medical devices are widely used in chronic implants and are generally perceived to be safe. However, immune-related complications including malignancies have recently been linked to textured breast implants. Here, we examine the influence of clinically approved breast implants surface features on host immune responses. Prosthetics with surface roughness of 0, 4, and 90 (Ra) were implanted in mammary fat pads of mice for 2 weeks and cells adjacent to the resulting tissue capsules were evaluated for foreign body immune responses using single-cell RNA-seq. Our findings identify a unique and finely tuned surface topography that is capable of modulating implant immunity to suppress foreign body response.

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Effect of hyperglycemia on the transcriptional profile of primary human macrophages

Project description:Hyperglycemia is an essential factor leading to micro- and macrovascular diabetic complications. Macrophages are key innate immune regulators of inflammation that undergo 2 major directions of functional polarization: classically (M1) and alternatively (M2) activated macrophages. The aim of the study was to examine the effect of hyperglycemia on transcriptional activation of M0, M1 and M2 human macrophages.

2017-07-12 | GSE86298 | GEO

Control of the inflammatory macrophage transcriptional signature by miR-155

Project description:Classically activated (M1) macrophages protect from infection but can cause inflammatory disease and tissue damage while alternatively activated (M2) macrophages reduce inflammation and promote tissue repair. Modulation of macrophage phenotype may be therapeutically beneficial and requires further understanding of the molecular programs that control macrophage differentiation. A potential mechanism by which macrophages differentiate may be through microRNA (miRNA), which bind to messenger RNA and post-transcriptionally modify gene expression, cell phenotype and function. The inflammation-associated miRNA, miR-155, was rapidly up-regulated over 100-fold in M1, but not M2, macrophages. Inflammatory M1 genes and proteins iNOS, IL-1b and TNF-a were reduced up to 72% in miR-155 knockout mouse macrophages, but miR-155 deficiency did not affect expression of genes associated with M2 macrophages (e.g., Arginase-1). Additionally, a miR-155 oligonucleotide inhibitor efficiently suppressed iNOS and TNF-a gene expression in wild-type M1 macrophages. Comparative transcriptional profiling of unactivated (M0) and M1 macrophages derived from wild-type and miR-155 knockout (KO) mice revealed an M1 signature of approximately 1300 genes, half of which were dependent on miR-155. Real-Time PCR of independent datasets validated miR-155's contribution to induction of iNOS, IL-1b, TNF-a, IL-6 and IL-12, as well as suppression of miR-155 targets Inpp5d, Tspan14, Ptprj and Mafb. Overall, these data indicate that miR-155 plays an essential role in driving the differentiation and effector potential of inflammatory M1 macrophages. Total RNA was prepared from bone marrow-derived macrophages of miR-155 knockout mice (n=2 independent mice) treated in M0, M1 or M2 conditions (n=2 replicates per condition originating from different mice)

2016-07-15 | E-GEOD-77425 | biostudies-arrayexpress

Fibrin promotes oxidative stress and neuronal loss in traumatic brain injury via innate immune activation

Project description:Traumatic brain injury (TBI) causes significant blood-brain barrier (BBB) breakdown, resulting in the extravasation of blood proteins into the brain. The impact of blood proteins, especially fibrinogen, on inflammation and neurodegeneration post-TBI is not fully understood, highlighting a critical gap in our comprehension of TBI pathology and its connection to innate immune activation. We combined vascular casting with 3D imaging of solvent-cleared organs (uDISCO) to study the spatial distribution of the blood coagulation protein fibrinogen in large, intact brain volumes and assessed the temporal regulation of the fibrin(ogen) deposition by immunohistochemistry in a murine model of TBI. Fibrin(ogen) deposition and innate immune cell markers were co-localized by immunohistochemistry in mouse and human brains after TBI. We assessed the role of fibrinogen in TBI using unbiased transcriptomics, flow cytometry and immunohistochemistry for innate immune and neuronal markers in Fggγ390–396A knock-in mice, which express a mutant fibrinogen that retains normal clotting function, but lacks the γ390–396 binding motif to CD11b/CD18 integrin receptor. We show that cerebral fibrinogen deposits were associated with activated innate immune cells in both human and murine TBI. Genetic elimination of fibrin-CD11b interaction reduced peripheral monocyte recruitment and the activation of inflammatory and reactive oxygen species (ROS) gene pathways in microglia and macrophages after TBI. Blockade of the fibrin-CD11b interaction was also protective from oxidative stress damage and cortical loss after TBI. These data suggest that fibrinogen is a regulator of innate immune activation and neurodegeneration in TBI. Abrogating post-injury neuroinflammation by selective blockade of fibrin’s inflammatory functions may have implications for long-term neurologic recovery following brain trauma.

2024-04-16 | GSE253476 | GEO

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