Mesenchymal Wnt/β-catenin signaling induces Wnt and BMP antagonists in dental epithelium

Chen, Xiaoyan; Liu, Jing; Li, Nan; Wang, Yu; Zhou, Nan; Zhu, Lei; Shi, Yiding; Wu, Yingzhang; Xiao, Jing; Liu, Chao

doi:10.1080/15476278.2019.1633871

Cited by 16 publications

(12 citation statements)

References 26 publications

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“…41 Additionally, after the conditional removal of β-catenin from the mesenchyme, the tooth bud fails to attain the cap stage. 133 This phenomenon conforms with the observation that odontogenesis signals are transmitted from the epithelium to mesenchyme. Moreover, tooth development can be blocked by inhibiting Wnt signalling via decreasing the expression of the Wnt activator R-Spondin 3 or increasing the expression of the Wnt inhibitor, Dkkl.…”

Section: Tf Transcription Factorsupporting

confidence: 89%

Tooth number abnormality: from bench to bedside

Zhang

Gong

et al. 2023

Int J Oral Sci

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Tooth number abnormality is one of the most common dental developmental diseases, which includes both tooth agenesis and supernumerary teeth. Tooth development is regulated by numerous developmental signals, such as the well-known Wnt, BMP, FGF, Shh and Eda pathways, which mediate the ongoing complex interactions between epithelium and mesenchyme. Abnormal expression of these crutial signalling during this process may eventually lead to the development of anomalies in tooth number; however, the underlying mechanisms remain elusive. In this review, we summarized the major process of tooth development, the latest progress of mechanism studies and newly reported clinical investigations of tooth number abnormality. In addition, potential treatment approaches for tooth number abnormality based on developmental biology are also discussed. This review not only provides a reference for the diagnosis and treatment of tooth number abnormality in clinical practice but also facilitates the translation of basic research to the clinical application.

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Section: Tf Transcription Factorsupporting

confidence: 89%

Tooth number abnormality: from bench to bedside

Zhang

Gong

et al. 2023

Int J Oral Sci

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“…To confirm the sequencing results and the DEGs screened by RNA-seq data analysis, furthermore, the expression level of 2 DEGs ( Saa3 and Cxcl5 ) was assessed using qRT-PCR. The Saa3 and Cxcl5 genes might be potentially associated with cytoskeletal rearrangement ( 21 , 22 ). Furthermore, both of these genes showed high expression levels and significantly expressed differences among knockdown and expression groups.…”

Section: Resultsmentioning

confidence: 99%

“…β-catenin not only acts as a transducer that regulates canonical Wnt/β-catenin signaling but also is a crucial component that couples with actin-cytoskeleton (19). Several studies have validated the involvement of β-catenin in palatogenesis (20)(21)(22). Previous research focused mainly on the underlying mechanism of epithelial β-catenin in palatogenesis.…”

Section: Introductionmentioning

confidence: 99%

“…They revealed that epithelial β-catenin participates in palatal fusion by controlling the expression of transforming growth factor-β3 (TGFβ3) ( 20 ). Although early research reported that the cleft palate phenotype occurred when Wnt/β-catenin signaling was activated in palatal mesenchyme ( 21 , 22 ), further investigation has never been pursued. To clarify the precise mechanism, our team established a β-catenin knockout mouse model.…”

Section: Introductionmentioning

confidence: 99%

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Transcriptome sequencing analysis of the role of β-catenin in F-actin reorganization in embryonic palatal mesenchymal cells

Liu¹,

Lu²,

Shi³

et al. 2022

Ann Transl Med

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Background: Palatogenesis is a highly regulated and coordinated developmental process that is coordinated by multiple transcription factors and signaling pathways. Our previous studies identified that defective palatal shelf reorientation due to aberrant mesenchymal β-catenin signaling is associated with Filamentous actin (F-actin) dysregulation. Herein, the underlying mechanism of mesenchymal β-catenin in regulating F-actin cytoskeleton reorganization is further investigated.Methods: Firstly, β-catenin silenced and overexpressed mouse embryonic palatal mesenchymal (MEPM) cells were established by adenovirus-mediated transduction. Subsequently, we compared transcriptomes of negative control (NC) group, β-catenin knockdown (KD) group, or β-catenin overexpression group respectively using RNA-sequencing (RNA-seq), and differentially expressed genes (DEGs) screened were further identified by quantitative real-time polymerase chain reaction (qRT-PCR). Finally, in vivo experiments further verified the expression change of critical molecules. Results:We discovered 184 and 522 DEGs in the knockdown and overexpression groups compared to the NC group, respectively (adjusted P<0.05; |fold change| >2.0). Among these, 106 DEGs were altered in both groups. Gene Ontology (GO) enrichment analysis relating to biological functions identified cytokinecytokine receptor interaction, and positive modulation of cellular migration. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment assessment indicated that these DEGs were chiefly linked by the regulation of signaling receptor activity and chemokine signaling pathways. Quantitative real-time polymerase chain reaction (qRT-PCR) results showed that the similar expression trend of serum amyloid A3 (Saa3) and CXC-chemokine ligand 5 (Cxcl5) possibly involved in cytoskeletal rearrangement with RNA-seq data. Experiments in vivo displayed that no significant expression change of Saa3 and Cxcl5 was observed in β-catenin knockout and overexpressed mouse models. Conclusions:Our study provides an expression landscape of DEGs in β-catenin silenced and overexpressed MEPM cells, which emphasizes the important role of processes such as chemotactic factor and cell migration. Our data gain deeper insight into genes associated with F-actin reorganization that is regulated by β-catenin either directly or by another route, which will contribute to further investigation of the exact mechanism of mesenchymal β-catenin/F-actin in palatal shelf reorientation.

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“…Tunic cells can migrate during the whole embryonic development process, form a large number of aggregates, and migrate to the outer surface of the embryo to perform their functions (Bishop et al, 2010). In vertebrates, bone morphogenetic protein (Chen et al, 2019), fibroblast-binding factors (FGFs) (Sun and Stathopoulos, 2018), transforming growth factor beta (Hao et al, 2019), Wingless-type/β-catenin (Jarvinen et al, 2018;Chen et al, 2019), and other signaling pathways are involved in the differentiation of mesenchymal stem cells into diverse cell types, such as chondrocytes (Yang et al, 2018), odontogenic cells (Cui et al, 2018), and muscle cells (De Bari et al, 2003;Kumar et al, 2017). Also, miR-145 mediates the differentiation of mesenchymal cells into smooth muscle cells (Yeh et al, 2019), and mesenchymal stem cell-derived exosome miR-223 regulates neuronal cell apoptosis (Wei et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

A microRNA Cluster-Lefty Pathway is Required for Cellulose Synthesis During Ascidian Larval Metamorphosis

Sun

Zhang

Yang

et al. 2022

Front. Cell Dev. Biol.

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Synthesis of cellulose and formation of tunic structure are unique traits in the tunicate animal group. However, the regulatory mechanism of tunic formation remains obscure. Here, we identified a novel microRNA cluster of three microRNAs, including miR4018a, miR4000f, and miR4018b in Ciona savignyi. In situ hybridization and promoter assays showed that miR4018a/4000f/4018b cluster was expressed in the mesenchymal cells in the larval trunk, and the expression levels were downregulated during the later tailbud stage and larval metamorphosis. Importantly, overexpression of miR4018a/4000f/4018b cluster in mesenchymal cells abolished the cellulose synthesis in Ciona larvae and caused the loss of tunic cells in metamorphic larvae, indicating the regulatory roles of miR4018a/4000f/4018b cluster in cellulose synthesis and mesenchymal cell differentiation into tunic cells. To elucidate the molecular mechanism, we further identified the target genes of miR4018a/4000f/4018b cluster using the combination approaches of TargetScan prediction and RNA-seq data. Left–right determination factor (Lefty) was confirmed as one of the target genes after narrow-down screening and an experimental luciferase assay. Furthermore, we showed that Lefty was expressed in the mesenchymal and tunic cells, indicating its potentially regulatory roles in mesenchymal cell differentiation and tunic formation. Notably, the defects in tunic formation and loss of tunic cells caused by overexpression of miR4018a/4000f/4018b cluster could be restored when Lefty was overexpressed in Ciona larvae, suggesting that miR4018a/4000f/4018b regulated the differentiation of mesenchymal cells into tunic cells through the Lefty signaling pathway during ascidian metamorphosis. Our findings, thus, reveal a novel microRNA-Lefty molecular pathway that regulates mesenchymal cells differentiating into tunic cells required for the tunic formation in tunicate species.

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Mesenchymal Wnt/β-catenin signaling induces Wnt and BMP antagonists in dental epithelium

Cited by 16 publications

References 26 publications

Tooth number abnormality: from bench to bedside

Tooth number abnormality: from bench to bedside

Transcriptome sequencing analysis of the role of β-catenin in F-actin reorganization in embryonic palatal mesenchymal cells

A microRNA Cluster-Lefty Pathway is Required for Cellulose Synthesis During Ascidian Larval Metamorphosis

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