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Related Concept Videos

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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
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Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
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Reprograming Model of Human Monocyte-derived Macrophages for In-vitro Assays
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Reprogramming macrophage orientation by microRNA 146b targeting transcription factor IRF5.

Liang Peng1, Hui Zhang1, Yuanyuan Hao1

  • 1Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai,New York, NY 10029, United States.

Ebiomedicine
|November 10, 2016
PubMed
Summary
This summary is machine-generated.

Interleukin-10 (IL-10) regulates macrophage polarization via miR-146b, a microRNA targeting IRF5. This pathway is crucial for preventing intestinal inflammation and colitis development.

Keywords:
CRISPR/Cas9ColitisInterleukin 10MacrophagemiR-146b

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Area of Science:

  • Immunology
  • Molecular Biology
  • Gastroenterology

Background:

  • Macrophage polarization is critical in pathological conditions, yet its regulation remains unclear.
  • Interleukin-10 (IL-10) is a key immunoregulatory cytokine.
  • MicroRNAs (miRNAs) are emerging regulators of cellular processes, including inflammation.

Purpose of the Study:

  • To investigate the role of IL-10 in regulating macrophage orientation during inflammation.
  • To elucidate the specific molecular mechanisms, including miRNA involvement, linking IL-10 to macrophage polarization.
  • To evaluate the therapeutic potential of targeting this pathway in colitis.

Main Methods:

  • Utilized IL-10 and Rag1 double knockout mice to study spontaneous colitis.
  • Analyzed macrophage phenotype (M1 polarization) and cytokine expression.
  • Investigated the regulatory relationship between IL-10, miR-146b, and IRF5 using molecular biology techniques.
  • Assessed the therapeutic effect of miR-146b mimics in vivo models of colitis.

Main Results:

  • IL-10 deficiency led to spontaneous colitis with a dominant M1 macrophage phenotype.
  • IL-10 stimulation upregulated miR-146b expression, which targets IRF5 and regulates macrophage activation.
  • miR-146b deficiency exacerbated intestinal inflammation and M1 macrophage polarization.
  • Treatment with miR-146b mimics suppressed M1 macrophage activation and ameliorated colitis.

Conclusions:

  • IL-10 dependent miR-146b plays a significant role in modulating M1 macrophage orientation.
  • The IL-10/miR-146b/IRF5 axis is a critical regulator of intestinal inflammation.
  • Targeting miR-146b represents a potential therapeutic strategy for inflammatory bowel diseases like colitis.