Objective: To investigate a dysregulation of Notch signaling in oral lichen planus(OLP)using public available microarray dataset.Methods: A m RNA expression profiling dataset from Gene Expression Omnibus was downloade...Objective: To investigate a dysregulation of Notch signaling in oral lichen planus(OLP)using public available microarray dataset.Methods: A m RNA expression profiling dataset from Gene Expression Omnibus was downloaded. Differential gene expression between OLP and normal oral epithelium was examined using Network Analyst. The dysregulated genes related to Notch signaling were identified.Results: Thirteen genes in Notch signaling pathway were significantly differential expressed between OLP and normal epithelium. OLP samples significantly increased the m RNA levels of HEYL, APH1 B, CNTN1 and PSEN2. Whilst, ITCH, HES1, TLE2, DLK2,DTX2, NOTCH3, JAG2, RFNG, and SPEN were downregulated in OLP groups.Conclusions: Notch signaling was dysregulated and may participate in pathophysiologic process in OLP.展开更多
FAM83H mutations lead to autosomal dominant hypocalcified amelogenesis imperfecta(ADHCAI).However,the biological role of FAM83H remains unclear.The present study aimed to characterize the alveolar bone cells isolated ...FAM83H mutations lead to autosomal dominant hypocalcified amelogenesis imperfecta(ADHCAI).However,the biological role of FAM83H remains unclear.The present study aimed to characterize the alveolar bone cells isolated from a patient with ADHCAI having the mutation,c.1261G>T,p.E421*,in FAM83H.We showed that FAM83H mutant cells had proliferation ability and morphology similar to the controls.The F-actin staining revealed that FAM83H mutant cells were remained in the earlier stages of cell spreading compared to the controls at 30 min,but their spreading was advanced comparable to the controls at later stages.After osteogenic induction,a significant decrease in mRNA levels of RUNX2 and ALP was observed in FAM83H mutant cells at day 7 compared with day 3 while their expressions were increased in the controls.The OPN levels in FAM83H mutant cells were not significantly changed at day 7 compared to day 3 while the controls showed a significant increase.After 14 days,the mineral deposition of FAM83H mutant cells was slightly lower than that of the controls.In conclusion,we identify that FAM83H bone cells have lower expression of osteogenic marker genes and mineralization while they maintain their morphology,proliferation,and spreading.Consistent with previous studies in the ameloblasts and periodontal ligamental cells,these evidences propose that FAM83H influences osteogenic differentiation across different cell types in oral cavity.展开更多
基金supported by the Rachadapisek Sompote Fund for Postdoctoral Fellowship,Chulalongkorn University
文摘Objective: To investigate a dysregulation of Notch signaling in oral lichen planus(OLP)using public available microarray dataset.Methods: A m RNA expression profiling dataset from Gene Expression Omnibus was downloaded. Differential gene expression between OLP and normal oral epithelium was examined using Network Analyst. The dysregulated genes related to Notch signaling were identified.Results: Thirteen genes in Notch signaling pathway were significantly differential expressed between OLP and normal epithelium. OLP samples significantly increased the m RNA levels of HEYL, APH1 B, CNTN1 and PSEN2. Whilst, ITCH, HES1, TLE2, DLK2,DTX2, NOTCH3, JAG2, RFNG, and SPEN were downregulated in OLP groups.Conclusions: Notch signaling was dysregulated and may participate in pathophysiologic process in OLP.
基金The study was supported by the Medical Genomics Cluster of Chulalongkorn University,Chulalongkorn Academic Advancement Into Its 2nd Century Project,Newton Fund,and Thailand Research Fund(RSA6280001,DPG6180001,RSA6180019).Nunthawan Nowwarote is supported by the Ratchadapisek Sompote Fund for Postdoctoral Fellowship,Chulalongkorn University.We thank Trakarn Sookthonglarng and Yuttupong Kunchanapruek for blood collection,Lawan Boonprakong and Anucharte Sirjunbarl for microscope services.
文摘FAM83H mutations lead to autosomal dominant hypocalcified amelogenesis imperfecta(ADHCAI).However,the biological role of FAM83H remains unclear.The present study aimed to characterize the alveolar bone cells isolated from a patient with ADHCAI having the mutation,c.1261G>T,p.E421*,in FAM83H.We showed that FAM83H mutant cells had proliferation ability and morphology similar to the controls.The F-actin staining revealed that FAM83H mutant cells were remained in the earlier stages of cell spreading compared to the controls at 30 min,but their spreading was advanced comparable to the controls at later stages.After osteogenic induction,a significant decrease in mRNA levels of RUNX2 and ALP was observed in FAM83H mutant cells at day 7 compared with day 3 while their expressions were increased in the controls.The OPN levels in FAM83H mutant cells were not significantly changed at day 7 compared to day 3 while the controls showed a significant increase.After 14 days,the mineral deposition of FAM83H mutant cells was slightly lower than that of the controls.In conclusion,we identify that FAM83H bone cells have lower expression of osteogenic marker genes and mineralization while they maintain their morphology,proliferation,and spreading.Consistent with previous studies in the ameloblasts and periodontal ligamental cells,these evidences propose that FAM83H influences osteogenic differentiation across different cell types in oral cavity.
