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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Epigenetic Regulation01:46

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Introduction to Fibroblasts01:09

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Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
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Inheritance of Chromatin Structures03:17

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Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying...
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Histone Modification02:32

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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
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Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
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DNA methylation in fibrosis.

Christopher Dowson1, Steven O'Reilly1

  • 1Cell Biology Group, Faculty of Health and Life Sciences, Northumbria University, Ellison Building, Newcastle Upon Tyne NE1 3HY, United Kingdom.

European Journal of Cell Biology
|June 28, 2016
PubMed
Summary

DNA methylation abnormalities drive fibrosis by altering myofibroblast activation. These rapid, reversible epigenetic changes offer promising therapeutic targets for intractable fibrotic diseases.

Keywords:
FibrosisMethyl cap binding proteinMethylationPPARSystemic sclerosis

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Area of Science:

  • Epigenetics
  • Cell Biology
  • Pathology

Background:

  • Fibrosis is characterized by excessive extracellular matrix (ECM) production and myofibroblast activation.
  • Myofibroblasts, marked by alpha-smooth muscle actin, are key players in fibrotic conditions.
  • Current therapies for fibrosis are limited, representing a significant unmet clinical need.

Purpose of the Study:

  • To review the role of DNA methylation in fibroblast to myofibroblast activation.
  • To explore the potential of targeting methylation for fibrosis treatment.
  • To highlight the therapeutic potential of reversible epigenetic modifications in fibrotic diseases.

Main Methods:

  • Literature review focusing on epigenetic regulation in fibrosis.
  • Analysis of studies investigating DNA methylation patterns in fibrotic tissues.
  • Examination of the link between methylation, gene expression, and myofibroblast function.

Main Results:

  • Fibroblast activation into myofibroblasts appears to be under epigenetic control, specifically DNA methylation.
  • Aberrant DNA methylation patterns (hypermethylation and hypomethylation) are observed in various fibrotic conditions.
  • These methylation changes are rapid and reversible, suggesting therapeutic tractability.

Conclusions:

  • DNA methylation plays a critical role in the pathogenesis of fibrosis by regulating myofibroblast activation.
  • Targeting epigenetic mechanisms, particularly DNA methylation, presents a novel therapeutic strategy for fibrosis.
  • Further research into methylation-based therapies could address the urgent clinical need for effective fibrosis treatments.