BBS7–SHH Signaling Activity Regulates Primary Cilia for Periodontal Homeostasis

Chang, Pi En; Li, Shujin; Kim, Hyun-Yi; Lee, Dong-Joon; Choi, Yoon Jeong; Jung, Han‐Sung

doi:10.3389/fcell.2021.796274

Cited by 7 publications

(3 citation statements)

References 42 publications

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“…For PD, BBS7 is essential for periodontal ligament homeostasis through regulating primary cilia. BBS7 was downregulated in occlusal hypofunctional periodontal ligament, and knockdown of BBS7 could inhibit cell migration and angiogenesis ( Chang et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Discovering genetic linkage between periodontitis and type 1 diabetes: A bioinformatics study

et al. 2023

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Background: Relationship between periodontitis (PD) and type 1 diabetes (T1D) has been reported, but the detailed pathogenesis requires further elucidation. This study aimed to reveal the genetic linkage between PD and T1D through bioinformatics analysis, thereby providing novel insights into scientific research and clinical treatment of the two diseases.Methods: PD-related datasets (GSE10334, GSE16134, GSE23586) and T1D-related datasets(GSE162689)were downloaded from NCBI Gene Expression Omnibus (GEO). Following batch correction and merging of PD-related datasets as one cohort, differential expression analysis was performed (adjusted p-value <0.05 and ∣log2 fold change| > 0.5), and common differentially expressed genes (DEGs) between PD and T1D were extracted. Functional enrichment analysis was conducted via Metascape website. The protein-protein interaction (PPI) network of common DEGs was generated in The Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database. Hub genes were selected by Cytoscape software and validated by receiver operating characteristic (ROC) curve analysis.Results: 59 common DEGs of PD and T1D were identified. Among these DEGs, 23 genes were commonly upregulated, and 36 genes were commonly downregulated in both PD- and T1D-related cohorts. Functional enrichment analysis indicated that common DEGs were mainly enriched in tube morphogenesis, supramolecular fiber organization, 9 + 0 non-motile cilium, plasma membrane bounded cell projection assembly, glomerulus development, enzyme-linked receptor protein signaling pathway, endochondral bone morphogenesis, positive regulation of kinase activity, cell projection membrane and regulation of lipid metabolic process. After PPI construction and modules selection, 6 hub genes (CD34, EGR1, BBS7, FMOD, IGF2, TXN) were screened out and expected to be critical in linking PD and T1D. ROC analysis showed that the AUC values of hub genes were all greater than 70% in PD-related cohort and greater than 60% in T1D-related datasets.Conclusion: Shared molecular mechanisms between PD and T1D were revealed in this study, and 6 hub genes were identified as potential targets in treating PD and T1D.

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Section: Discussionmentioning

confidence: 99%

Discovering genetic linkage between periodontitis and type 1 diabetes: A bioinformatics study

et al. 2023

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“…Hematoxylin and eosin (HE) staining was performed after deparaffinization. For immunological staining of histological sections or cells, the following antibodies were used, as previously described [ 46 ]. Rabbit anti-CACNA1C (1:200, Alomone Labs, ACC-003), mouse anti-CK14 (1:500, Abcam, ab7800), mouse anti-CK10 (1:500, Invitrogen, MA5-13705), mouse anti-E-cadherin (1:500, BD Biosciences, AF748), rabbit anti-MMP-9 (1:200, Merck, AB19016), rabbit anti-LGR5 (1:200, Abcam, ab75732), mouse anti-Ki67 (1:200, Abcam, ab16667), mouse anti-PCNA (1:500, Abcam, ab29), mouse anti-NFATc1 (1:200, Santa Cruz, SC-7294), and mouse anti-β-catenin (1:500, Santa Cruz, SC-7963).…”

Section: Methodsmentioning

confidence: 99%

Unraveled roles of Cav1.2 in proliferation and stemness of ameloblastoma

Lee

Kim³

et al. 2022

Cell Biosci

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Background Transcriptome analysis has been known as a functional tool for cancer research recently. Mounting evidence indicated that calcium signaling plays several key roles in cancer progression. Despite numerous studies examining calcium signaling in cancer, calcium signaling studies in ameloblastoma are limited. Results In the present study, comparative transcriptome profiling of two representative odontogenic lesions, ameloblastoma and odontogenic keratocyst, revealed that Cav1.2 (CACNA1C, an L-type voltage-gated calcium channel) is strongly enriched in ameloblastoma. It was confirmed that the Ca2+ influx in ameloblastoma cells is mainly mediated by Cav1.2 through L-type voltage-gated calcium channel agonist and blocking reagent treatment. Overexpression and knockdown of Cav1.2 showed that Cav1.2 is directly involved in the regulation of the nuclear translocation of nuclear factor of activated T cell 1 (NFATc1), which causes cell proliferation. Furthermore, a tumoroid study indicated that Cav1.2-dependent Ca2+ entry is also associated with the maintenance of stemness of ameloblastoma cells via the enhancement of Wnt/β-catenin signaling activity. Conclusion In conclusion, Cav1.2 regulates the NFATc1 nuclear translocation to enhance ameloblastoma cell proliferation. Furthermore, Cav1.2 dependent Ca2+ influx contributes to the Wnt/β-catenin activity for the ameloblastoma cell stemness and tumorigenicity. Our fundamental findings could have a major impact in the fields of oral maxillofacial surgery, and genetic manipulation or pharmacological approaches to Cav1.2 can be considered as new therapeutic options.

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“…In fetal enamel organs, the primary cilium is expressed in enamel knots, which are signaling centers that signal mesenchymal tissues [ 117 ]. In other tooth-related tissues, the hypofunctional periodontal ligament (PDL) downregulates the expression of BBS7 by delaying cell migration and suppressing cell angiogenesis [ 141 ]. Recent studies have shown that the primary cilium has a close relationship not only with Hh, but also with WNT [ 142 ], fibroblast growth factor (FGF) [ 143 ], and PDGF [ 144 ].…”

Section: Hedgehog Signaling and Ciliopathymentioning

confidence: 99%

Hedgehog-Related Mutation Causes Bone Malformations with or without Hereditary Gene Mutations

Onodera,

Azuma

2023

IJMS

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The hedgehog (Hh) family consists of numerous signaling mediators that play important roles at various stages of development. Thus, the Hh pathway is essential for bone tissue development and tumorigenesis. Gorlin syndrome is a skeletal and tumorigenic disorder caused by gain-of-function mutations in Hh signaling. In this review, we first present the phenotype of Gorlin syndrome and the relationship between genotype and phenotype in bone and craniofacial tissues, including the causative gene as well as other Hh-related genes. Next, the importance of new diagnostic methods using next-generation sequencing and multiple gene panels will be discussed. We summarize Hh-related genetic disorders, including cilia disease, and the genetics of Hh-related bone diseases.

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BBS7–SHH Signaling Activity Regulates Primary Cilia for Periodontal Homeostasis

Cited by 7 publications

References 42 publications

Discovering genetic linkage between periodontitis and type 1 diabetes: A bioinformatics study

Discovering genetic linkage between periodontitis and type 1 diabetes: A bioinformatics study

Unraveled roles of Cav1.2 in proliferation and stemness of ameloblastoma

Hedgehog-Related Mutation Causes Bone Malformations with or without Hereditary Gene Mutations

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