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Mismatch Repair01:36

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Mismatch Repair01:20

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Capturing Tissue Repair in Zebrafish Larvae with Time-lapse Brightfield Stereomicroscopy
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Eicosanoids in tissue repair.

Julia Esser-von Bieren1

  • 1Center of Allergy and Environment (ZAUM), Technical University of Munich and Helmholtz Center Munich, 80802, Munich, Germany.

Immunology and Cell Biology
|January 26, 2019
PubMed
Summary
This summary is machine-generated.

Eicosanoids, lipid mediators from arachidonic acid, are crucial for tissue repair. Understanding their roles in healing and disease can lead to new therapies for chronic wounds and scarring.

Keywords:
Arachidonic acidinflammationleukotrieneslipid mediatorsprostaglandinstype 2 immunity

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Area of Science:

  • Biomedical Science
  • Molecular Biology
  • Immunology

Background:

  • Tissue damage from trauma or infection requires orchestrated repair for homeostasis.
  • Lipid mediators, eicosanoids, are key regulators of tissue repair processes.
  • Dysregulated tissue repair contributes to pathological conditions like chronic wounds, scarring, and fibrosis.

Purpose of the Study:

  • To review the current understanding of eicosanoid functions in tissue repair during health and disease.
  • To explore the temporal, cellular, and tissue-specific production of eicosanoids during repair.
  • To discuss therapeutic strategies targeting eicosanoids for improved tissue regeneration.

Main Methods:

  • Literature review of eicosanoid roles in tissue repair.
  • Analysis of eicosanoid production mechanisms.
  • Discussion of pathological repair contexts and therapeutic potential.

Main Results:

  • Eicosanoids exhibit versatile roles in regulating tissue repair.
  • Eicosanoid production is tightly controlled in a time-, cell-, and tissue-dependent manner.
  • Specific eicosanoids have distinct roles in epithelial barrier repair and pathological conditions.

Conclusions:

  • Eicosanoids are critical mediators in physiological and pathological tissue repair.
  • Targeting eicosanoid pathways offers potential for therapeutic interventions.
  • Future strategies aim to promote healing and prevent adverse outcomes like scarring and tissue dysfunction.