TRIM16 Promotes Osteogenic Differentiation of Human Periodontal Ligament Stem Cells by Modulating CHIP-Mediated Degradation of RUNX2

Zhao, Yi; Zhai, Qiaoli; Liu, Hong; Xi, Xun; Chen, Shuai; Li, Dongxu

doi:10.3389/fcell.2020.625105

Cited by 13 publications

(21 citation statements)

References 51 publications

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“…A study has shown that TRIM16 and Galectin-3 coregulate the osteogenic differentiation of hBMSCs [ 49 ]. Furthermore, TRIM16 reduces CHIP, which reduces CHIP-mediated RUNX2 degradation, thus promoting osteogenic differentiation of hPDLSCs [ 50 ].…”

Section: Effect Of E3 Ubiquitin Ligases In Skeletal Cell Fate and Pat...mentioning

confidence: 99%

E3 Ubiquitin Ligases: Potential Therapeutic Targets for Skeletal Pathology and Degeneration

Zeng

Xiong

Lin

et al. 2022

Stem Cells International

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The ubiquitination-proteasome system (UPS) is crucial in regulating a variety of cellular processes including proliferation, differentiation, and survival. Ubiquitin protein ligase E3 is the most critical molecule in the UPS system. Dysregulation of the UPS system is associated with many conditions. Over the past few decades, there have been an increasing number of studies focusing on the UPS system and how it affects bone metabolism. Multiple E3 ubiquitin ligases have been found to mediate osteogenesis or osteolysis through a variety of pathways. In this review, we describe the mechanisms of UPS, especially E3 ubiquitin ligases on bone metabolism. To date, many E3 ubiquitin ligases have been found to regulate osteogenesis or osteoclast differentiation. We review the classification of these E3 enzymes and the mechanisms that influence upstream and downstream molecules and transduction pathways. Finally, this paper reviews the discovery of the relevant UPS inhibitors, drug molecules, and noncoding RNAs so far and prospects the future research and treatment.

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Section: Effect Of E3 Ubiquitin Ligases In Skeletal Cell Fate and Pat...mentioning

confidence: 99%

E3 Ubiquitin Ligases: Potential Therapeutic Targets for Skeletal Pathology and Degeneration

Zeng

Xiong

Lin

et al. 2022

Stem Cells International

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“…Ring finger protein 185 inhibits the WNT signaling pathway by promoting the ubiquitination and degradation of Dvl2, thus negatively regulating osteogenic differentiation (Zhou et al, 2014). Tripartite motif (TRIM) 16 was found to stabilize RUNX2 by reducing the CHIPmediated ubiquitination and degradation of K48-linked RUNX2, thereby promoting the osteogenic differentiation of human periodontal ligament stem cells (Zhao et al, 2020). TRIM21 was reported to promote the K48-linked ubiquitination of AKT, which accelerated the degradation of AKT to inhibit the osteotropic signaling pathway, thus inhibiting the osteogenic differentiation of MSCs (Xian et al, 2022).…”

Section: Other E3 Ligasesmentioning

confidence: 99%

Ubiquitin modification in osteogenic differentiation and bone formation: From mechanisms to clinical significance

Pan

Tang

et al. 2022

Front. Cell Dev. Biol.

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The ubiquitin–proteasome system is an important pathway for mediating posttranslational modification and protein homeostasis and exerts a wide range of functions in diverse biological processes, including stem cell differentiation, DNA repair, and cell cycle regulation. Many studies have shown that ubiquitination modification plays a critical role in regulating the osteogenic differentiation of stem cells and bone formation through various mechanisms. This review summarizes current progress on the effects and mechanisms of ubiquitin modification on transcription factors and signaling pathways involved in osteogenic differentiation. Moreover, the review highlights the latest advances in the clinical application of drugs in bone tissue engineering. A thorough understanding of ubiquitin modifications may provide promising therapeutic targets for stem cell-based bone tissue engineering.

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“…After 36 hours transfection of HEK293 cells or after 14 days odontogenic differentiation of hDPSCs, total RNA was isolated using Trizol reagent (Invitrogen) and reverse transcribed into cDNA using the PrimeScript™ RT reagent Kit (Takara, China). These genes primers have been published elsewhere [43,44]. Gene expression levels were calculated using the (2 -ΔΔCT ) method.…”

Section: Quantitative Real-time Polymerase Chain Reactionmentioning

confidence: 99%

Whole Exome Sequencing Identifies a Novel COL1A1 Missense Mutation Causing Dentinogenesis Imperfecta Type I Without Skeletal Abnormalities

Zeng¹,

Pan²,

Mo³

et al. 2021

Preprint

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Background：Osteogenesis imperfecta (OI) is a genetic disorder characterized by bone fragility, blue sclerae and dentinogenesis imperfecta (DGI), which are mainly caused by a mutation of the COL1A1 or COL1A2 genes that encode type I procollagen.Methods: The ultrastructure of dentin was analyzed by micro-CT, scanning electron microscopy, energy-dispersive spectroscopy analysis, nanoindentation test and Toluidine Blue Staining. Whole-exome sequencing (WES) was performed to identify the pathogenic gene. The function of the mutant COL1A1 was studied by real-time PCR, western blotting, subcellular localization. Functional analysis in dental pulp stem cells (DPSCs) was also performed to explore the impact of the identified mutation on this phenotype. Results: WES identified a missense mutation (c.1463G > C) in exon 22 of the COL1A1 gene. However, the cases reported herein only exhibited DGI-I in the clinical phenotype, there is no bone disease and any other common abnormal symptom caused by COL1A1 mutation. In addition, ultrastructural analysis of the tooth affected with non-syndromic DGI-I showed that the abnormal dentin was accompanied by disruption of odontoblast polarization, reduced numbers of odontoblasts, loss of dentinal tubules, and reduction in hardness and elasticity, suggesting severe developmental disturbance. What’s more, the odontoblast differentiation ability based on DPSCs that were isolated and cultured from the DGI-I patient was enhanced compared with those from an age-matched, healthy control.Conclusion: This study helped the family members to understand the disease progression and provided new insights into the phenotype-genotype association in collagen-associated diseases and improve clinical diagnosis of OI/DGI-I.

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TRIM16 Promotes Osteogenic Differentiation of Human Periodontal Ligament Stem Cells by Modulating CHIP-Mediated Degradation of RUNX2

Cited by 13 publications

References 51 publications

E3 Ubiquitin Ligases: Potential Therapeutic Targets for Skeletal Pathology and Degeneration

E3 Ubiquitin Ligases: Potential Therapeutic Targets for Skeletal Pathology and Degeneration

Ubiquitin modification in osteogenic differentiation and bone formation: From mechanisms to clinical significance

Whole Exome Sequencing Identifies a Novel COL1A1 Missense Mutation Causing Dentinogenesis Imperfecta Type I Without Skeletal Abnormalities

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