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Promoter-Specific Hypomethylation Correlates with IL-1β Overexpression in Tuberous Sclerosis Complex (TSC)

A. Fuso, AM. Iyer, J. van Scheppingen, M. Maccarrone, T. Scholl, JA. Hainfellner, M. Feucht, FE. Jansen, WG. Spliet, P. Krsek, J. Zamecnik, A. Mühlebner, E. Aronica,

. 2016 ; 59 (4) : 464-70. [pub] 20160428

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc17013906
E-zdroje Online Plný text

NLK ProQuest Central od 1997-02-01 do Před 1 rokem
Medline Complete (EBSCOhost) od 1997-02-01 do Před 1 rokem
Health & Medicine (ProQuest) od 1997-02-01 do Před 1 rokem
Psychology Database (ProQuest) od 1997-02-01 do Před 1 rokem

Odkazy

PubMed 27122151
DOI 10.1007/s12031-016-0750-7
Knihovny.cz E-zdroje

In tuberous sclerosis complex (TSC), overexpression of numerous genes associated with inflammation has been observed. Among different proinflammatory cytokines, interleukin-1β (IL-1β) has been shown to be significantly involved in epileptogenesis and maintenance of seizures. Recent evidence indicates that IL-1β gene expression can be regulated by DNA methylation of its promoter. In the present study, we hypothesized that hypomethylation in the promoter region of the IL-1β gene may underlie its overexpression observed in TSC brain tissue. Bisulfite sequencing was used to study the methylation status of the promoter region of the IL-1β gene in TSC and control samples. We identified hypomethylation in the promoter region of the IL-1β gene in TSC samples. IL-1β is overexpressed in tubers, and gene expression is correlated with promoter hypomethylation at CpG and non-CpG sites. Our results provide the first evidence of epigenetic modulation of the IL-1β signaling in TSC. Thus, strategies that target epigenetic alterations could offer new therapeutic avenues to control the persistent activation of interleukin-1β-mediated inflammatory signaling in TSC brain.

Citace poskytuje Crossref.org

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