JHDM1D and HDAC1–3 mRNA expression levels in perip

Authors: MJ Nawrocki AJ Strugała P Piotrowski M Wudarski M Olesińska PP Jagodziński

Publish Date: 2015/11/12

Volume: 74, Issue: 10, Pages: 902-910

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Abstract

Systemic lupus erythematosus SLE is a chronic relapsing autoimmune disease characterized by production of autoantibodies against a series of nuclear antigens and by chronic inflammation The etiology of SLE is the result of interactions between genetic epigenetic hormonal and environmental factors Changes in histone acetylation and methylation contribute to structural chromatin modificationsWe studied the histone demethylase JHDM1D and histone deacetylases HDAC1 HDAC2 and HDAC3 transcript levels in peripheral blood mononuclear cells PBMCs from patients diagnosed with systemic lupus erythematosus SLE Furthermore the association of JHDM1D HDAC1 HDAC2 and HDAC3 transcript levels with gender age and major clinical manifestations were analyzedSignificantly lower HDAC2 transcript levels p = 0006785 and significantly higher JHDM1D p = 00000002 and HDAC1 p = 0010581 transcript levels in SLE patients were observed compared with healthy controls Higher JHDM1D mRNA expression was detected in active SLE patients when compared with inactive patients p = 0005 Furthermore the JHDM1D transcript levels were positively correlated with disease activity r s = 0368 p = 0045 while HDAC2 mRNA expression was positively correlated with disease duration r s = 0502 p = 00047Our analyses confirmed the importance of epigenetic alterations histone demethylation and acetylation in SLE etiology Moreover our results suggest that the presence of some clinical manifestations like hematological disease and antiRo antibody might be associated with the dysregulation of histone demethylase and deacetylases mRNA expression levelsDer systemische Lupus eythematodes SLE ist eine rezidivierende chronische Autoimmunerkrankung welche durch die Produktion von Autoantikörpern gegen eine Reihe von nukleären Antigenen sowie durch chronische Entzündung charakterisiert ist Die Ätiologie des SLE ist das Ergebnis von Interaktionen zwischen genetischen epigenetischen hormonellen und Umweltfaktoren Veränderungen in der HistonAcetylation und Methylation tragen zu strukturellen ChromatinModifikationen beiWir untersuchten die Transkriptionslevel der HistonDemethylase JHDM1D sowie der HistonDeacetylasen HDAC1 HDAC2 und HDAC3 in peripheren mononukleären Blutzellen PBMC bei Patienten mit diagnostiziertem SLE Des Weiteren wurde der Zusammenhang der JHDM1D HDAC1 HDAC2 und HDAC3Transkriptionslevel mit Geschlecht Alter und wichtigen klinischen Manifestationen analysiert

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