Abstract
A chronic inflammatory condition of gastric mucosa can facilitate the influx of new stem cells into the stomach. Epigenetic codes, such as DNA methylation, may be responsible for the stable maintenance of epigenetic phenotypes established in the new stomach-adapted stem cells. A number of hypotheses have been made for the role of CpG-island methylation, which is common in the Helicobacter pylori-infected stomach. However, they could not explain the plausible role of CpG-island methylation in the re-establishment of epigenetic phenotypes. These islands are highly repetitive sequences densely methylated throughout the human genome, the so-called parasitic retroelements, which expand a number of cDNA copies with reverse transcriptase. The densely methylated retroelements adjacent to the host genes can form the transitional-CpG sites around gene-control regions that are barely methylated. This review focuses on the putative role of transitional CpG methylation in the adaptive differentiation of new stem cells in the H. pylori-infected stomach.
Financial & competing interests disclosure
This work was supported by the Catholic Medical Center Research Foundation made in the program year of 2011 (5-2011-B0001-00029). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.