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Related Concept Videos

Experimental RNAi02:15

Experimental RNAi

RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
MicroRNAs01:22

MicroRNAs

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...
MicroRNAs01:22

MicroRNAs

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Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
siRNA - Small Interfering RNAs02:30

siRNA - Small Interfering RNAs

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Related Experiment Video

Updated: Jul 17, 2026

Using RNA-interference to Investigate the Innate Immune Response in Mouse Macrophages
12:47

Using RNA-interference to Investigate the Innate Immune Response in Mouse Macrophages

Published on: November 3, 2014

Gene silencing in severe systemic inflammation.

Charles E McCall1, Barbara K Yoza

  • 1Section of Molecular Medicine, Department of Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1042, USA. chmccall@wfubmc.edu

American Journal of Respiratory and Critical Care Medicine
|January 27, 2007
PubMed
Summary

Gene expression reprogramming silences inflammatory genes in severe systemic inflammation, unlike localized conditions. This epigenetic mechanism offers potential new treatments for critical care patients.

Related Experiment Videos

Last Updated: Jul 17, 2026

Using RNA-interference to Investigate the Innate Immune Response in Mouse Macrophages
12:47

Using RNA-interference to Investigate the Innate Immune Response in Mouse Macrophages

Published on: November 3, 2014

Area of Science:

  • Critical Care Medicine
  • Molecular Biology
  • Immunology

Background:

  • Severe systemic inflammation, including systemic inflammatory response syndrome (SIRS), sepsis, and septic shock, involves complex gene expression changes.
  • Localized inflammatory processes, such as rheumatoid arthritis, exhibit different gene expression patterns compared to systemic inflammation.
  • Understanding gene reprogramming in inflammation is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To appraise the concept of gene expression reprogramming in inflammatory diseases.
  • To emphasize the role of gene silencing in severe systemic inflammation and the SIRS continuum.
  • To explore the clinical and basic science context of gene silencing during SIRS.

Main Methods:

  • Review and synthesis of current literature on gene reprogramming in inflammatory diseases.
  • Analysis of gene silencing mechanisms, including the "nuclear factor-kappaB paradox" and epigenetic modifications.
  • Discussion of the potential clinical implications of gene silencing compartmentalization.

Main Results:

  • Gene reprogramming that silences acute proinflammatory genes is a key feature of severe systemic inflammation (SIRS continuum).
  • This silencing is not observed in localized inflammatory conditions like rheumatoid arthritis.
  • Epigenetic mechanisms involving nucleosome modifications and RelB expression contribute to gene silencing.

Conclusions:

  • Emergent understanding of gene silencing in SIRS provides a novel framework for treatment development.
  • Targeting gene reprogramming offers a potential therapeutic avenue for critical care conditions characterized by severe systemic inflammation.
  • Further research into the compartmentalization of gene silencing may reveal specific therapeutic targets.