Comprehensive analysis of transcription factors involved in odontoblast differentiation mechanism.
Haruka NakazatoShoko OnoderaNatsuko AidaMasahiro FurusawaToshifumi AzumaPublished in: Medical molecular morphology (2024)
Primary cultured odontoblasts rapidly lose their tissue-specific phenotype. To identify transcription factors (TF) that are important for the maintenance of the odontoblast phenotype, primary cultures of C57BL/6 J mouse dental mesenchymal cells (DMC) were isolated, and expression of TF and odontoblast marker genes in cells immediately after isolation and 2 days after culture were comprehensively evaluated and compared using RNA-sequencing (RNA-seq). The expression of odontoblast markers in mouse dental mesenchymal cells decreased rapidly after isolation. In addition, the expression of Hedgehog-related, Notch-related, and immediate- early gene (IEG)-related transcription factors significantly decreased. Forced expression of these genes in lentiviral vectors, together with fibroblast growth factor 4 (FGF4), fibroblast growth factor 9 (FGF9), and the Wnt pathway activator CHIR99021, significantly induced the expression of odontogenic marker genes. These results indicate, for the first time, that Notch signaling and early genes may be important for maintaining odontoblast cultures. Furthermore, simultaneous stimulation of FGF, Wnt, Hedgehog, Notch pathways, and IEG transcription factors cooperatively promoted the maintenance of the odontoblast phenotype. These results suggest that the Hedgehog and Notch signaling pathways may play an important role in maintaining odontoblast phenotypes, in addition to FGF and Wnt signaling.
Keyphrases
- transcription factor
- poor prognosis
- genome wide identification
- induced apoptosis
- stem cells
- genome wide
- rna seq
- cell proliferation
- single cell
- cell cycle arrest
- signaling pathway
- binding protein
- bone marrow
- gene expression
- endoplasmic reticulum stress
- long non coding rna
- bioinformatics analysis
- oxidative stress
- pi k akt
- copy number
- epithelial mesenchymal transition
- genome wide analysis
- drug induced
- high glucose
- toll like receptor
- gene therapy