Abstract:
Inflammatory bowel disease (IBD) is characterized by the infiltration of inflammatory cells
culminating in non-functional intestinal barrier. Despite the exponential increase of IBD
prevalence worldwide, there is no cure yet. Previous studies reported that inflammatory
milieu in human colon augments the expression of intercellular complexes called
connexins to facilitate homocellular and heterocellular communication. Moreover, in the
same context, epigenetic key players such as TET2 have shown to be upregulated in order
to facilitate DNA demethylation process of different genes involved. In this study, we
investigated the variation of the expression of Cx43 and TET2 in a DSS-induced colitis
mouse model and after gap junction blockade. Under inflammatory conditions, Cx43 and
TET2 expression levels were increased to be then reduced back to normal when followed
by gap junctions’ inhibition. Furthermore, TET2 function does not seem to be affected
since 5-hmc accumulation does not vary significantly upon inflammation nor GJ blockade.
These results show that Cx43 and TET2 may have a potential role in IBD pathogenesis.
Finally, Cx43 can be a potential therapeutic target for IBD treatments.
