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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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Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Immunostaining for DNA Modifications: Computational Analysis of Confocal Images
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DNA demethylation increases NETosis.

Hiroyuki Yasuda1, Yutaka Takishita1, Akihiro Morita1

  • 1Department of Biochemistry, Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, 3500-3, Minamitamagaki, Suzuka-city, Mie, 513-8670, Japan.

Archives of Biochemistry and Biophysics
|June 21, 2020
PubMed
Summary
This summary is machine-generated.

Epigenetic changes, specifically DNA demethylation, enhance neutrophil extracellular trap (NET) formation, a process called NETosis. This finding links epigenetics to diseases involving NETosis, like autoimmune conditions and cancer.

Keywords:
DNA methylationHistone citrullinationNETosisNeutrophil extracellular trapPeptidylarginine deiminase 4

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Area of Science:

  • Immunology
  • Epigenetics
  • Cell Biology

Background:

  • Neutrophil extracellular traps (NETs) and NETosis are implicated in autoimmune diseases, cancer, and diabetes.
  • Epigenetic regulation, particularly DNA methylation, is known to influence these diseases but its role in NETosis was unexplored.

Purpose of the Study:

  • To investigate the impact of epigenetic modifications, specifically DNA demethylation, on NETosis.
  • To explore the relationship between DNA demethylation, peptidylarginine deiminase 4 (PAD4) expression, and NETosis.

Main Methods:

  • Utilized HL-60 cells differentiated into neutrophil-like cells with DMSO.
  • Applied 5-azacytidine (Aza), a DNA methyltransferase (DNMT) inhibitor, during differentiation to induce DNA demethylation.
  • Assessed NETosis induction with and without A23187 (calcium ionophore).
  • Measured reactive oxygen species (ROS) production, mitochondrial ROS, DNA methylation status, and expression of PAD4 and citrullinated histone H3.

Main Results:

  • DNA demethylation induced by Aza enhanced spontaneous NETosis in neutrophil-like cells.
  • Aza treatment decreased ROS production but still promoted NETosis, suggesting a ROS-independent pathway.
  • Demethylation correlated with increased PAD4 expression and histone citrullination, key events in NETosis.
  • PAD4 inhibition partially reduced Aza-induced NETosis.

Conclusions:

  • DNA demethylation, triggered by DNMT inhibition, enhances NETosis in neutrophil-like cells.
  • This epigenetic regulation of NETosis involves increased PAD4 expression and histone citrullination.
  • The study establishes a novel link between epigenetics and NETosis, suggesting a mechanism for disease exacerbation in epigenetically influenced conditions.