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Effect of iodide ions on gene expression during M1 polarization of RAW264.7 macrophages.

ABSTRACT: To study the effect of iodide ions on the M1 polarization of macrophages, we chose the RAW264.7 cell line. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different groups.

ORGANISM(S): Mus musculus

PROVIDER: GSE230444 | GEO | 2024/06/27

REPOSITORIES: GEO

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Effect of iodide ions on gene expression during M1 polarization of RAW264.7 macrophages.

Project description:Effect of iodide ions on gene expression during M1 polarization of RAW264.7 macrophages.

| PRJNA961144 | ENA

Expression profiles of M1-polarized RAW264.7 cells [RAW_M1vsM0_RNA-seq]

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to evaluate the gene expression of M1-polarized RAW264.7 cells compared with M0 RAW264.7 cells. Methods: RAW264.7 cells were polarized toward M1 using LPS and IFN-γ. M0 RAW264.7 cells were maintained in culture without LPS and IFN-γ. Total RNA of M1 and M0 RAW264.7 cells was extracted. RAW264.7 cells RNA profiles were generated by deep sequencing for two groups (M1 versus M0 RAW264.7 cells) with three samples each. Results: There were significant differences between M1 and M0 RAW264.7 cells. Conclusions: Polarization of RAW264.7 cells from M0 to M1 induces various changes at the transcription level.

2024-03-31 | GSE183077 | GEO

Anti-inflammatory role of low intensity pulsed ultrasound in inhibiting LPS-induced M1 polarization of RAW264.7 via Wnt2b/AXIN/β-catenin

Project description:Low-intensity pulsed ultrasound (LIPUS) is a special type of low intensity ultrasound. In periodontal disease, LIPUS was applied as an adjuvant and non-invasive therapeutic treatment. While, the specific mechanism of LIPUS in the treatment of periodontal disease is not quite clear.RAW264.7 cells were induced to M1/M2 macrophage-like polarization by LPS/IL4. LIPUS was performed to stimulate RAW264.7 cells at an intensity of 45 mW/cm2, 25 min, interval 24 h, twice. The polyA mRNA sequencing of LPS induced RAW264.7 cells, LPS induced and LIPUS treated RAW264.7 cells were conducted.Our results suggested that LIPUS played an anti-inflammatory role by inhibiting LPS-induced M1 polarization of RAW264.7 cells in an Wnt2b/AXIN/β-catenin dependent way. LIPUS may inhibit inflammation in periodontal diseases by regulating macrophage differentiation, so as to play a therapeutic role in periodontal diseases.

2024-10-15 | GSE273466 | GEO

Expression profiles of M1-polarized RAW264.7 cells [RAW_M1vsM0_RNA-seq]

Project description:Expression profiles of M1-polarized RAW264.7 cells [RAW_M1vsM0_RNA-seq]

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miRNA profiling in RAW264.7 cells treated without or with LPS and IFNγ

Project description:We have identified a number of miRNAs that are differentially expressed in LPS and IFNγ treated RAW264.7 cells, as compared to untreated cells. Microarray and quantitative real-time PCR (qRT-PCR) results showed that miR-103 decreased while the STAT1 expression increased substantially in RAW264.7 derived M1 macrophage, and there was a significant negative correlation between miR-103 and STAT1.Overexpression of miR-103 suppressed M1 polarization by inhibiting STAT1/IRF1 signaling pathway and vice versa in vitro. STAT1 is a direct target of of miR-103.

2020-10-28 | GSE143845 | GEO

Myeloid cell derived inducible nitric oxide synthase suppresses M1 macrophage polarization

Project description:Analysis of gene expression between WT and iNOS defecient M1 macrophage RNA microarray was performed using RNA isolated from M1 polarized macrophages from WT and iNOS deficient mice stimulated with LPS/IFNγ for 6 hours. Total RNA was extracted using a RNeasy plus kit (QIAGEN, Valencia, CA), and the array was performed on an Illumina MouseRef-8 v2.0 expression beadchip (Illumina, USA) by the Genomics Core Facility at the Mount Sinai School of Medicine.

2015-02-02 | E-GEOD-65436 | biostudies-arrayexpress

Differential gene expression analysis of iodide treated rat thyroid follicular cell line PCCl3

Project description:The inhibitory effect of supra physiological iodide concentrations on thyroid hormone synthesis (Wolff-Chaikoff effect) and thyrocyte proliferation is largely know as iodine autoregulation. However, the molecular mechanisms by which iodide excess modulate thyroid functions remains unclear. In this work, we analyzed the rat follicular cell PCCl3 transcriptome profile under untreated and treated conditions with 10-3M sodium iodide (Na/I). Serial Analysis of Gene Expression revealed several transcripts differentially expressed in response to the iodide showing that excess iodide affects almost all aspects of thyroid cell function and differentiation acting on the iodine autoregulatory mechanism through a complex process. Keywords: comparative genomic analysis

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Iodide Inhibits Vascular Endothelial Growth Factor-A Expression in Cultured Human Thyroid Follicles

Project description:A Microarray Search for Effects of Thyrotropin and Iodide on Angiogenesis Factors Objective: Excess iodide has been administered to hyperthyroid patients before thyroid surgery to reduce intraoperative bleeding and oozing. The purpose of this study was to elucidate the mechanism by which iodide reduces blood flow in the hypervascular thyroid gland. Design: Human thyroid follicles were cultured in the presence or absence of thyrotropin (TSH), or in medium containing various concentrations of iodide, and TSH- or iodide-regulated gene expression was analyzed by cDNA microarray. Main outcome: TSH stimulated the expression of thyroglobulin, peroxidase, sodium-iodide symporter, vascular endothelial growth factor (VEGF)-A, VEGF-B, and placental growth factor (PGF) but decreased that of VEGF-C by half. When thyroid follicles were cultured in high-iodide (10-5M) medium, TSH-induced expression of VEGF-A, VEGF-B and PGF was decreased, accompanied by a reduction of VEGF-A release into the medium. Furthermore, expression of putative angiogenesis inhibitors such as urokinase-type plasminogen activator (PLAU) was increased. These findings were confirmed by real-time polymerase chain reaction (PCR) and Northern blot hybridization. Conclusions: We have demonstrated for the first time that iodide at high concentration decreases the expression of the angiogenic factors VEGF-A, VEGF-B, and PGF, accompanied by an increase in the expression of possible anti-angiogenic factors such as PLAU. These proangiogenic and antiangiogenic factors may at least partly account for the iodide-induced decrease in thyroid blood flow.

2008-08-01 | GSE12244 | GEO

RNA editing enzyme APOBEC3A promotes pro-inflammatory (M1) macrophage polarization

Project description:Macrophages acquire a pro-inflammatory M1 phenotype in response to microbial products or pro-inflammatory cytokines through incompletely understood molecular mechanisms. We recently described the induction of APOBEC3A-mediated cellular site-specific cytosine-to-uracil (C>U) RNA editing during M1 macrophage polarization. However, the functional significance of this RNA editing is unknown. Here, we find that cellular RNA editing by APOBEC3A can also be induced by influenza or Maraba virus infections in normal macrophages, and by interferons in tumor-associated macrophages. Gene knockdown and RNA Seq analyses show that APOBEC3A induces C>U RNA editing (range 7%-88%) of 209 exonic or UTR sites in 203 genes during M1 polarization of monocyte-derived macrophages. The highest level of deleterious protein-recoding C>U RNA editing is observed in THOC5, which encodes a key nuclear protein implicated in the export of mRNAs during M-CSF driven macrophage differentiation. Knockdown of APOBEC3A in M1 macrophages reduces pro-inflammatory IL6, IL23A, and IL12B gene expression, CD80 and CD86 surface protein expression, and TNF-α, IL-1β and IL-6 cytokine secretion, and increases glycolysis and glycolytic capacity. These results demonstrate that APOBEC3A cytidine deaminase plays an important role in transcriptomic and functional polarization of pro-inflammatory M1 macrophages.

2020-03-13 | GSE146867 | GEO

Transcriptional response of thyroid to iodide in wild-type and Nrf2 knockout mice

Project description:Analysis of differentially expressed mRNAs indicated that iodide overload upregulated inflammatory-, immune-, fibrosis- and oxidative stress-related pathways, including the Nrf2 pathway. Nrf2 KO mice showed a more pronounced inflammatory-autoimmune transcriptional response to iodide

2020-08-31 | GSE157121 | GEO

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