The Wnt Antagonist SFRP1: A Key Regulator of Periodontal Mineral Homeostasis

Gopinathan, Gokul; Foyle, Deborah; Diekwisch, Thomas G.H.

doi:10.1089/scd.2019.0124

Cited by 27 publications

(34 citation statements)

References 32 publications

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“…Subpopulations of periodontal MSCs indeed maintain for long time a highly migratory behavior, which has been hypothesized to depend as well on the peculiar periodontal microenvironment ( Diekwisch, 2002 ; Luan et al., 2009 ). Microenvironmental cues would then result in the generation of different mesenchymal cell and stem cell populations via induction of vast epigenetic alterations ( Gopinathan et al., 2019 ; Luan et al., 2009 ), thus modulating MSC behavior and determining their identity in the dental pulp and periodontium both during development and in adult life.…”

Section: Discussionmentioning

confidence: 99%

A single-cell atlas of human teeth

et al. 2021

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Section: Discussionmentioning

confidence: 99%

A single-cell atlas of human teeth

et al. 2021

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“…The following references appear in the Supplemental Information: Bao and Jin, 2006 , Byrd and Meyers, 2005 , Chen et al., 2012 , Chen et al., 2014 , Coles et al., 2006 , Dixon et al., 1994 , Duprez et al., 1999 , Fukumoto et al., 2006 , Gammill et al., 2006 , Gopinathan et al., 2019 , Hargrave et al., 1997 , Hill et al., 2014 , Huang et al., 2016 , Humphreys et al., 2012 , Jia et al., 2016 , Kamalakar et al., 2019 , Li et al., 2009 , Li et al., 2018 , Micaglio et al., 2019 , Nikopoulos et al., 2007 , Parada et al., 2015 , Pilia et al., 1999 , Roosenboom et al., 2018 , Sela-Donenfeld and Kalcheim, 1999 , Shin et al., 2012 , Sock et al., 2004 , Teng et al., 2017 , Toyofuku et al., 2008 , Wang and Astrof, 2016 , Wu and Taneyhill, 2012 , Yen et al., 2010 , York et al., 2018 , Yu and Moens, 2005 , Zhang et al., 2016 , Zhu et al., 2019 , Zuniga et al., 2010 .…”

Section: Supporting Citationsmentioning

confidence: 99%

Functional Diversification of SRSF Protein Kinase to Control Ubiquitin-Dependent Neurodevelopmental Signaling

et al. 2020

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Summary Conserved protein kinases with core cellular functions have been frequently redeployed during metazoan evolution to regulate specialized developmental processes. The Ser/Arg (SR)-rich splicing factor (SRSF) protein kinase (SRPK), which is implicated in splicing regulation, is one such conserved eukaryotic kinase. Surprisingly, we show that SRPK has acquired the capacity to control a neurodevelopmental ubiquitin signaling pathway. In mammalian embryonic stem cells and cultured neurons, SRPK phosphorylates Ser-Arg motifs in RNF12/RLIM, a key developmental E3 ubiquitin ligase that is mutated in an intellectual disability syndrome. Processive phosphorylation by SRPK stimulates RNF12-dependent ubiquitylation of nuclear transcription factor substrates, thereby acting to restrain a neural gene expression program that is aberrantly expressed in intellectual disability. SRPK family genes are also mutated in intellectual disability disorders, and patient-derived SRPK point mutations impair RNF12 phosphorylation. Our data reveal unappreciated functional diversification of SRPK to regulate ubiquitin signaling that ensures correct regulation of neurodevelopmental gene expression.

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“…To maintain physiologic alveolar bone levels, mesenchymal stem cells (MSCs) from the periodontal ligament (PDL), periodontal blood vessel pericytes, and alveolar bone progenitors jointly contribute to the renewal of alveolar bone (Pacios et al 2015; Zhou et al 2016; Luan et al 2017). The continuous recruitment and differentiation of mesenchymal progenitors for the renewal of alveolar bone are essential for periodontal bone homeostasis (Diekwisch 2019; Gopinathan et al 2019). One of the very first genes involved in alveolar bone osteogenic lineage commitment in the periodontal region is the runt-related transcription factor 2 (Runx2; Luan et al 2009), and its expression is epigenetically controlled by the histone demethylase JARID1D1B/KDM5B (Rojas et al 2015).…”

Section: Histone Methylation and Odontoblastogenesis/osteoblastogenesismentioning

confidence: 99%

Histone Methylation: Achilles Heel and Powerful Mediator of Periodontal Homeostasis

et al. 2020

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The packaging of DNA around nucleosomes exerts dynamic control over eukaryotic gene expression either by granting access to the transcriptional machinery in an open chromatin state or by silencing transcription via chromatin compaction. Histone methylation modification affects chromatin through the addition of methyl groups to lysine or arginine residues of histones H3 and H4 by means of histone methyl transferases or histone demethylases. Changes in histone methylation state modulate periodontal gene expression and have profound effects on periodontal development, health, and therapy. At the onset of periodontal development, progenitor cell populations such as dental follicle cells are characterized by an open H3K4me3 chromatin mark on RUNX2, MSX2, and DLX5 gene promoters. During further development, periodontal progenitor differentiation undergoes a global switch from the H3K4me3 active methyl mark to the H3K27me3 repressive mark. When compared with dental pulp cells, periodontal neural crest lineage differentiation is characterized by repressive H3K9me3 and H3K27me3 marks on typical dentinogenesis-related genes. Inflammatory conditions as they occur during periodontal disease result in unique histone methylation signatures in affected cell populations, including repressive H3K9me3 and H3K27me3 histone marks on extracellular matrix gene promoters and active H3K4me3 marks on interleukin, defensin, and chemokine gene promoters, facilitating a rapid inflammatory response to microbial pathogens. The inflammation-induced repression of chromatin on extracellular matrix gene promoters presents a therapeutic opportunity for the application of histone methylation inhibitors capable of inhibiting suppressive trimethylation marks. Furthermore, inhibition of chromatin coregulators through interference with key inflammatory mediators such as NF-kB by means of methyltransferase inhibitors provides another avenue to halt the exacerbation of the inflammatory response in periodontal tissues. In conclusion, histone methylation dynamics play an intricate role in the fine-tuning of chromatin states during periodontal development and harbor yet-to-be-realized potential for the treatment of periodontal disease.

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The Wnt Antagonist SFRP1: A Key Regulator of Periodontal Mineral Homeostasis

Cited by 27 publications

References 32 publications

A single-cell atlas of human teeth

A single-cell atlas of human teeth

Functional Diversification of SRSF Protein Kinase to Control Ubiquitin-Dependent Neurodevelopmental Signaling

Histone Methylation: Achilles Heel and Powerful Mediator of Periodontal Homeostasis

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