2-Hydroxyethyl methacrylate (HEMA),a tooth filling material, was proven to have toxic effects on different cell types, including human gingival fibroblasts (HGFs), and to be able to influence odontoblast vitality. The aim of the present study was to assess the differential transcriptome modulation induced by low HEMA concentration in cultured HGFs. RNA extracted from cultured HGFs exposed to 3 mmol/l HEMA for 24 or 96 h underwent a whole genome microarray analysis. Data analysis showed the presence of two gene clusters, composed by 310 transcripts differentially expressed after 24- and 96-h HEMA treatment compared to controls. Functional analysis demonstrated that these transcripts are mainly involved in cellular survival and death, and inflammatory response. The study highlighted an overall damage induced by HEMA exposure at both 24 and 96 h, mainly leading to a proliferation impairment. Interestingly, 24-h HEMA treatment seems to induce the cells to trigger repair mechanisms, evidencing an early compensatory response, whereas 96-h incubation appears to cause the occurrence of apoptosis as a consequence of the chronic damage.

Transcriptome modifications in human gingival fibroblasts exposed to 2-hydroxyethyl methacrylate

DI NISIO, Chiara
Primo
;
D'AURORA, MARCO;DI GIACOMO, Viviana;STUPPIA, Liborio;CATALDI, Amelia;GATTA, Valentina
Ultimo
2016-01-01

Abstract

2-Hydroxyethyl methacrylate (HEMA),a tooth filling material, was proven to have toxic effects on different cell types, including human gingival fibroblasts (HGFs), and to be able to influence odontoblast vitality. The aim of the present study was to assess the differential transcriptome modulation induced by low HEMA concentration in cultured HGFs. RNA extracted from cultured HGFs exposed to 3 mmol/l HEMA for 24 or 96 h underwent a whole genome microarray analysis. Data analysis showed the presence of two gene clusters, composed by 310 transcripts differentially expressed after 24- and 96-h HEMA treatment compared to controls. Functional analysis demonstrated that these transcripts are mainly involved in cellular survival and death, and inflammatory response. The study highlighted an overall damage induced by HEMA exposure at both 24 and 96 h, mainly leading to a proliferation impairment. Interestingly, 24-h HEMA treatment seems to induce the cells to trigger repair mechanisms, evidencing an early compensatory response, whereas 96-h incubation appears to cause the occurrence of apoptosis as a consequence of the chronic damage.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11564/653623
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