BACKGROUND: As environmental factors appear to predispose patients to hidradenitis suppurativa (HS), studying epigenetic modifications is of interest to further understand the pathogenesis of HS. OBJECTIVES: To study the expression of DNA hydroxymethylation regulators, namely the ten-eleven translocation (TET) and isocitrate dehydrogenase (IDH) family, in the skin of HS patients. MATERIALS & METHODS: Twenty patients with HS and 12 healthy subjects were recruited. We analysed the expression of TET1, TET2, TET3, IDH1, IDH2, IDH3a, and IDH3b in lesional and perilesional HS tissue as well as tissue from healthy controls by quantitative real-time reverse transcription polymerase chain reaction (RT-PCR). In addition, immunohistochemistry was performed for TET1, TET2, and TET3. RESULTS: RT-PCR analysis showed that mRNA of all the studied genes was significantly under-expressed in lesional HS skin compared to healthy skin. IDH1 and IDH2 mRNA expression was also significantly lower in perilesional HS skin compared to healthy skin, and TET3 mRNA expression was significantly lower in lesional HS skin compared to perilesional HS skin. RT-PCR analysis for TET1, TET2, and TET3 mRNA expression was confirmed by immunohistochemical analysis. Correlation analysis revealed a significant positive correlation between TET and IDH gene expression in perilesional and lesional HS skin. CONCLUSIONS: Our results suggest that epigenetic changes occur in HS tissue and that aberrant expression of the DNA hydroxymethylation regulators may play a role in the pathogenesis of HS. As epigenetic modifications are reversible, further research into the cause of these aberrant expression patterns is warranted in order to develop possible novel therapeutic approaches.
BACKGROUND: As environmental factors appear to predispose patients to hidradenitis suppurativa (HS), studying epigenetic modifications is of interest to further understand the pathogenesis of HS. OBJECTIVES: To study the expression of DNA hydroxymethylation regulators, namely the ten-eleven translocation (TET) and isocitrate dehydrogenase (IDH) family, in the skin of HS patients. MATERIALS & METHODS: Twenty patients with HS and 12 healthy subjects were recruited. We analysed the expression of TET1, TET2, TET3, IDH1, IDH2, IDH3a, and IDH3b in lesional and perilesional HS tissue as well as tissue from healthy controls by quantitative real-time reverse transcription polymerase chain reaction (RT-PCR). In addition, immunohistochemistry was performed for TET1, TET2, and TET3. RESULTS: RT-PCR analysis showed that mRNA of all the studied genes was significantly under-expressed in lesional HS skin compared to healthy skin. IDH1 and IDH2 mRNA expression was also significantly lower in perilesional HS skin compared to healthy skin, and TET3 mRNA expression was significantly lower in lesional HS skin compared to perilesional HS skin. RT-PCR analysis for TET1, TET2, and TET3 mRNA expression was confirmed by immunohistochemical analysis. Correlation analysis revealed a significant positive correlation between TET and IDH gene expression in perilesional and lesional HS skin. CONCLUSIONS: Our results suggest that epigenetic changes occur in HS tissue and that aberrant expression of the DNA hydroxymethylation regulators may play a role in the pathogenesis of HS. As epigenetic modifications are reversible, further research into the cause of these aberrant expression patterns is warranted in order to develop possible novel therapeutic approaches.