Project description:Objective: 2-Hydroxyethyl methacrylate (HEMA), one of the most common components of tooth filling materials, could diffuse throughout dentine, and in gingival and pulp cells, affecting odontoblast vitality. Design: the aim of this study was to assess the differential transcriptome modulation induced by HEMA treatment in human cultured gingival fibroblasts (HGFs) at different exposure time compared to untreated cells. Materials and methods: Gene expression profile was performed by employing a whole gene microarray approach on RNA extracted from cultured HGFs exposed to 3 mmol/l HEMA for 24 or 96 h. Differentially identified transcripts were analyzed by Ingenuity Pathways Analysis software to disclose genes biological functions. Results: Hierarchical clustering analysis of the data set originated from a total of 8 experiments showed the selective presence of two gene clusters, composed by hundreds trandcripts differentially expressed after 24-h and 96-h HEMA treatment. when compared to untreated controls. Functional analysis showed the transcripts involvement mainly in cell survival, proliferation and death, with an unbalance towards cell growth and inflammatory response. Conclusions: Data analysis showed an overall damage induced by HEMA exposure for both HGFs cultures at 24 and 96-h mainly leading to a proliferation impairement. Interestingly 24-h HEMA exposure could induce the cells to trigger repair mechanisms evidencing an early compensatory response and survive while. 96-h incubation might increase apoptosis as a consequence of the chronic damage. Gene expression profile of Human Gingival Fibroblasts (HGFs) exposed to 3mM 2-Hydroxyethyl Methacrylate (HEMA) for 24- and 96-h versus untreated Human Gingival Fibroblasts at 24- and 96-h. A total of 8 experiments was carried out including biological and technical replicates.
Project description:Objective: 2-Hydroxyethyl methacrylate (HEMA), one of the most common components of tooth filling materials, could diffuse throughout dentine, and in gingival and pulp cells, affecting odontoblast vitality. Design: the aim of this study was to assess the differential transcriptome modulation induced by HEMA treatment in human cultured gingival fibroblasts (HGFs) at different exposure time compared to untreated cells. Materials and methods: Gene expression profile was performed by employing a whole gene microarray approach on RNA extracted from cultured HGFs exposed to 3 mmol/l HEMA for 24 or 96 h. Differentially identified transcripts were analyzed by Ingenuity Pathways Analysis software to disclose genes biological functions. Results: Hierarchical clustering analysis of the data set originated from a total of 8 experiments showed the selective presence of two gene clusters, composed by hundreds trandcripts differentially expressed after 24-h and 96-h HEMA treatment. when compared to untreated controls. Functional analysis showed the transcripts involvement mainly in cell survival, proliferation and death, with an unbalance towards cell growth and inflammatory response. Conclusions: Data analysis showed an overall damage induced by HEMA exposure for both HGFs cultures at 24 and 96-h mainly leading to a proliferation impairement. Interestingly 24-h HEMA exposure could induce the cells to trigger repair mechanisms evidencing an early compensatory response and survive while. 96-h incubation might increase apoptosis as a consequence of the chronic damage.
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
Project description:Asthma is a chronic inflammatory airway disease characterized by airway inflammation and remodeling. The role of 15-oxo-5Z,8Z,11Z,13E-eicosatetraenoic acid (15-oxoETE), a 15-HETE metabolite catalyzed by 15-prostaglandin dehydrogenase (15-PGDH), has been relatively unexplored in asthma. In this study, we used RNA-seq to explore the effect of 15-KETE on the transcriptome of airway epithelial cells, aiming to identify its potential downstream targets and mechanisms of action.
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.