Objectives: Sex hormone receptors are reported to be present in human dental pulp (HDP) cells. The purpose of this study was to examine the biological significance of estrogen and androgen receptors (ER and AR, respectively) in HDP cells. Design: We isolated HDP cells expressing ER- and AR-mRNAs and investigated the expression status of the receptors and the response to sex hormones in the cells. Results: HDP cells expressing ER- and/or AR-mRNAs had the ability to form alizarin red S-positive nodules in which calcium and phosphorus were deposited in vitro and to differentiate into odontoblasts-like cells and dentin-like tissue in vivo. Individual clones isolated from HDP cells exhibited a different expression pattern of mRNA for ER and AR. Some clones expressed ER- and/or ER-mRNAs and the others coexpressed ER- and AR-mRNAs. Using the Ingenuity software, we found that 17-estradiol (E2) and dihydrotestosterone (DHT) could act directly on HDP cells through ER- or androgen signaling-mediated mechanisms. E2 or DHT stimulated the mRNA expression for genes related to odontogenesis of dentin-containing teeth and odontoblast differentiation, suggesting that ER and AR in HDP cells may be involved in dentinogenesis. Conclusions: Our findings provide new insights into the biological significance of sex hormone receptors in HDP cells.
Expression status of mRNA for sex hormone receptors in human dental pulp cells and the response to sex hormones in the cells.
Sex, Specimen part, Treatment
View SamplesExcessive MS is known to result in disappearance of the alveolar hard line, enlargement of thePDL space, and destruction of alveolar bone, leading to occlusal traumatism. The regulatory role of MS is believed to play a critical role in the process of alveolar bone remodeling. However, little is known about the effect of excessive MS on expression of osteoclastogenesis-related genes in human PDL cells.
Hyperocclusion stimulates osteoclastogenesis via CCL2 expression.
Age, Specimen part
View SamplesWe performed expression profiling of 36 types of normal human tissues and identified 2,503 tissue-specific genes. We then systematically studied the expression of these genes in cancers by re-analyzing a large collection of published DNA microarray datasets. Our study shows that integration of each gene's breadth of expression (BOE) in normal tissues is important for biological interpretation of the expression profiles of cancers in terms of tumor differentiation, cell lineage and metastasis.
Interpreting expression profiles of cancers by genome-wide survey of breadth of expression in normal tissues.
No sample metadata fields
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A Smad3 and TTF-1/NKX2-1 complex regulates Smad4-independent gene expression.
Specimen part, Cell line, Treatment
View SamplesWe determined and analyzed the effect of TTF-1/NKX2-1 on Smad3/Smad4 binding sites by ChIP-sequencing.
A Smad3 and TTF-1/NKX2-1 complex regulates Smad4-independent gene expression.
Specimen part, Cell line
View SamplesTTF-1/NKX2-1 was expressed by adenoviral vector and changes in gene expression were determined by RNA-sequencing. Overall design: A549 cells were infected with Ad-TTF-1 or Ad-LacZ vectors and stimulated with TGF-beta for 24 hours or left untreated. Expression of polyA RNA was determined.
A Smad3 and TTF-1/NKX2-1 complex regulates Smad4-independent gene expression.
No sample metadata fields
View SamplesLbetaT2 cells exposed to different number and concentration of GnRH pulses over 4 hours during in vitro perfusion culture
Pulse sensitivity of the luteinizing hormone beta promoter is determined by a negative feedback loop Involving early growth response-1 and Ngfi-A binding protein 1 and 2.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
ChIP-seq reveals cell type-specific binding patterns of BMP-specific Smads and a novel binding motif.
Specimen part, Cell line, Treatment
View SamplesSmad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing.
ChIP-seq reveals cell type-specific binding patterns of BMP-specific Smads and a novel binding motif.
Specimen part, Treatment
View SamplesSmad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing. We used expression microarrays to compare the Smad1/5 binding sites identified by ChIP-seq to BMP-induced gene expressions.
ChIP-seq reveals cell type-specific binding patterns of BMP-specific Smads and a novel binding motif.
Specimen part, Treatment
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