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The effects of fluoride on the gene expression of enamel forming ameloblasrs

ABSTRACT: We compared the overall gene expression pattern between secretory ameloblasts and maturation ameloblasts, and found out there were 244 genes differentially exppressed in the maturation ameloblasts as compared to secretory ameloblasts. Upon treatment, the genes coregulated with MMP-20 were downregulated in maturation ameloblasts, though the difference was not significant.

ORGANISM(S): Mus musculus

PROVIDER: GSE57224 | GEO | 2014/05/02

SECONDARY ACCESSION(S): PRJNA245933

REPOSITORIES: GEO

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The effects of fluoride on the gene expression of enamel forming ameloblasrs

Project description:We compared the overall gene expression pattern between secretory ameloblasts and maturation ameloblasts, and found out there were 244 genes differentially exppressed in the maturation ameloblasts as compared to secretory ameloblasts. Upon treatment, the genes coregulated with MMP-20 were downregulated in maturation ameloblasts, though the difference was not significant. Stage specific secretory ameloblasts (SAB) and maturation ameloblasts (MAB) were laser microdissected from mandibular incisors of control and 50 ppm F treated mice.

2014-05-02 | E-GEOD-57224 | biostudies-arrayexpress

Gene expression fingerprinting of ameloblasts shows changes in the endocytosis/cytoskeleton interface across stages.

Project description:We used RNA-seq to identify differentially expressed genes across ameloblast stages in rats. We found expression patterns of enamel matrix proteins, ion channels and transporters, and endocytosis regulators such as clathrin to match those found in previous experimental studies on ameloblasts. We hypothesized that ameloblasts change their endocytotic pathways as they progress from stage and stage, and we sought to identify novel patterns in expression of genes at the endocytosis/cytoskeleton interface. We found that maturation ameloblasts preferentially express synaptojanin 1 and intersectin 2 and secretory ameloblasts preferentially express Numb protein and amphiphysin. We also uncovered differential alternative splicing of ECI genes across ameloblast populations. In pointing to endocytotic genes hitherto unexplored in ameloblasts that also regulate cell morphology, this bioinformatics study suggests a mechanism by which cervical loop, secretory, and maturation ameloblasts switch modes of endocytosis in order to express genes that better suit the distinct morphology of each cell stage.

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MEMO1 is required for ameloblast maturation and functional enamel formation

Project description:Coordinated mineralization of soft tissue is central to organismal form and function, while dysregulated mineralization underlies several human pathologies. Oral epithelial derived ameloblasts are polarized, secretory cells responsible for generating enamel, the most mineralized substance in the human body. Defects in ameloblast development result in enamel anomalies, including amelogenesis imperfecta. Identifying proteins critical in ameloblast development can provide insight into specific pathologies associated with enamel related disorders or more broadly, mechanisms of mineralization. Previous studies identified a role for MEMO1 in bone mineralization; however, whether MEMO1 functions in the generation of additional mineralized structures remains unknown. Here, we identify a critical role for MEMO1 in enamel mineralization. First, we identified that Memo1 is expressed in ameloblasts and that conditional deletion of Memo1 from ameloblasts results in enamel defects, characterized by a decline in mineral density and tooth integrity. Molecular profiling of ameloblasts and their progenitors in Memo1 oral epithelial mutants revealed a disruption to cytoskeletal associated genes and a reduction in late stage ameloblast markers, relative to controls. Histology revealed that the molecular defects correlated with a disruption of the apical Tome’s process and the basolateral interacting, papillary layer, in Memo1 mutant ameloblasts. Finally, deletion of Memo1 from an oral epithelial ameloblast cell line, followed by cellular and molecular analyses, revealed altered cytoskeletal networks, relative to control cells. Collectively, our findings integrate MEMO1 into an emerging network of molecules important for ameloblast development and provide both in vivo and in vitro systems to further interrogate the relationship of cytoskeletal and amelogenesis-related defects.

2023-08-03 | GSE235869 | GEO

Human iPSC Derived Enamel Organoid Guided by Single Cell Atlas of Human Tooth Development

Project description:Tooth enamel secreted by ameloblasts is the hardest material in the human body, acting as a shield protecting the teeth. However, enamel is gradually damaged or partially lost in over 90% of adults and cannot be regenerated due to a lack of ameloblasts in erupted teeth. Here we use sci-RNA-seq to establish a spatiotemporal single cell atlas for the developing human tooth and identify regulatory mechanisms controlling the differentiation process of human ameloblasts. We reveal key signaling pathways involved between the support cells and ameloblasts during fetal development and recapitulate those findings in a novel human ameloblast in vitro differentiation from iPSCs. We furthermore develop a mineralizing enamel organ-like 3D organoid system. These studies pave the way for future regenerative dentistry and therapies toward genetic diseases affecting enamel formation.

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Transcriptome of human odontoblast, pre-secretory ameloblast and secretory ameloblast

Project description:The goal of the study was to characterize the whole genome transcriptome profiles of human ameloblasts and odontoblasts, evaluate molecular pathways and advance our knowledge of the human tooth development. We found that during primary tooth formation, odontoblasts expressed 14,802 genes, presecretory ameloblasts 15,179 genes and secretory ameloblasts 14,526 genes. Four human fetuses were obtained at ages 15-20 weeks gestation, immediately placed on ice and the tooth buds dissected from the jaws, placed in RNAlater and refrigerated at 4C for 1-4 weeks to allow decalcification by EDTA. The tissue was then frozen and stored at -80C. The tissue was sectioned at -35C at a thickness of 7 microns. These sections were used for laser capture microdissection (LCM) to isolate the human odontoblasts and ameloblasts in different stages of enamel formation, using static image settings. In total, 4 odontoblast, 4 pre-secretory ameloblast and 4 secretory ameloblast pooled samples were used for RNA extraction and microarray analysis.

2014-11-14 | E-GEOD-63289 | biostudies-arrayexpress

Transcriptome of human odontoblast, pre-secretory ameloblast and secretory ameloblast

2014-11-14 | GSE63289 | GEO

G-protein coupled receptor Gpr115 (Adgrf4) is required for enamel mineralization mediated by ameloblasts

Project description:Dental enamel, the hardest tissue in the human body, is derived from dental epithelial cell ameloblast-secreted enamel matrices. Enamel mineralization occurs in a strictly synchronized manner along with ameloblast maturation in association with ion transport and pH balance, and any disruption of these processes results in enamel hypomineralization. G-protein coupled receptors (GPCRs) function as transducers of external signals by activating associated G-proteins and regulate cellular physiology. Tissue-specific GPCRs play important roles in organ development, though their activities in tooth development remains poorly understood. The present results show that the adhesion-GPCR Gpr115 (Adgrf4) is highly and preferentially expressed in mature ameloblasts and plays a crucial role during enamel mineralization. To investigate the in vivo function of Gpr115, knockout (Gpr115-KO) mice were created and found to develop hypo-mineralized enamel, with a larger acidic area due to the dysregulation of ion composition. Transcriptomic analysis also revealed that deletion of Gpr115 disrupted pH homeostasis and ion transport processes in enamel formation. In addition, in vitro analyses using the dental epithelial cell line Cervical Loop-Derived Dental Epithelial (CLDE) cell demonstrated that Gpr115 is indispensable for the expression of carbonic anhydrase 6 (Car6), which has a critical role in enamel mineralization. Furthermore, an acidic condition induced Car6 expression under the regulation of Gpr115 in CLDE cells. Thus, we concluded that Gpr115 plays an important role in enamel mineralization via regulation of Car6 expression in ameloblasts. The present findings indicate a novel function of Gpr115 in ectodermal organ development and clarify the molecular mechanism of enamel formation.

2020-08-31 | GSE155641 | GEO