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  • Wang, Xijun  (4)
  • 1
    Online Resource
    Online Resource
    Napabucasin Induces Mouse Bone Loss by Impairing Bone Formation via STAT3
    Frontiers Media SA ; 2021
    In:  Frontiers in Cell and Developmental Biology Vol. 9 ( 2021-3-18)
    Details
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 9 ( 2021-3-18)
    Abstract: The novel small molecule Napabucasin (also known as BBI608) was shown to inhibit gene transcription driven by Signal Transducer and Activator of Transcription 3 (STAT3), which is considered a promising anticancer target. Many preclinical studies have been conducted in cancer patients examining the selective targeting of cancer stem cells by Napabucasin, but few studies have examined side effects of Napabucasin in the skeleton system. In the present study, we found treating bone marrow mesenchymal stem cells (BMSCs) with Napabucasin in vitro impaired their osteogenic differentiation. In terms of mechanisms, Napabucasin disrupted differentiation of BMSCs by inhibiting the transcription of osteogenic gene osteocalcin (Ocn) through STAT3. Moreover, through micro-CT analysis we found 4 weeks of Napabucasin injections induced mouse bone loss. Histological analysis revealed that Napabucasin-induced bone loss in mice was the result of impaired osteogenesis. In conclusion, this study provided evidence for the effect of Napabucasin on mouse bone homeostasis and revealed its underlying mechanisms in vivo and in vitro .
    Type of Medium: Online Resource
    ISSN: 2296-634X
    URL: Article
    DOI: 10.3389/fcell.2021.648866
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2737824-X
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  • 2
    Online Resource
    Online Resource
    ScRNA ‐seq links dental fibroblasts heterogeneity with mechanoresponsiveness
    Wiley ; 2023
    In:  Journal of Periodontal Research Vol. 58, No. 4 ( 2023-08), p. 800-812
    Details
    In: Journal of Periodontal Research, Wiley, Vol. 58, No. 4 ( 2023-08), p. 800-812
    Abstract: Periodontal ligament (PDL) and dental pulp (DP) share a common origin but have distinct biological and mechanical functions. To what extent the mechanoresponsive property of PDL can be attributed to its unique transcriptional profiles of cellular heterogeneity is unclear. This study aims to decipher cellular heterogeneity and distinct mechanoresponsive characteristics of odontogenic soft tissues and their underlying molecular mechanisms. Materials and Methods A single‐cell comparison of digested human periodontal ligament (PDL) and dental pulp (DP) was performed using scRNA‐seq. An in vitro loading model was constructed to measure mechanoresponsive ability. Dual‐luciferase assay, overexpression, and shRNA knockdown were used to investigate the molecular mechanism. Results Our results demonstrate striking fibroblast heterogeneity across and within human PDL and DP. We demonstrated that a tissue‐specific subset of fibroblasts existed in PDL exhibiting high expression of mechanoresponsive extracellular matrix (ECM) genes, which was verified by an in vitro loading model. ScRNA‐seq analysis indicated a particularly enriched regulator in PDL‐specific fibroblast subtype, Jun Dimerization Protein 2 (JDP2). Overexpression and knockdown of JDP2 extensively regulated the downstream mechanoresponsive ECM genes in human PDL cells. The force loading model demonstrated that JDP2 responded to tension and that knockdown of JDP2 effectively inhibited the mechanical force–induced ECM remodeling. Conclusions Our study constructed the PDL and DP ScRNA‐seq atlas to demonstrate PDL and DP fibroblast cellular heterogeneity and identify a PDL‐specific mechanoresponsive fibroblast subtype and its underlying mechanism.
    Type of Medium: Online Resource
    ISSN: 0022-3484 , 1600-0765
    URL: Issue
    URL: Article
    DOI: 10.1111/jre.v58.4
    DOI: 10.1111/jre.13139
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2025633-4
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  • 3
    Online Resource
    Online Resource
    Osteoblastic STAT3 Is Crucial for Orthodontic Force Driving Alveolar Bone Remodeling and Tooth Movement
    Wiley ; 2023
    In:  Journal of Bone and Mineral Research Vol. 38, No. 1 ( 2023-01), p. 214-227
    Details
    In: Journal of Bone and Mineral Research, Wiley, Vol. 38, No. 1 ( 2023-01), p. 214-227
    Abstract: Mechanical force is essential to shape the internal architecture and external form of the skeleton by regulating the bone remodeling process. However, the underlying mechanism of how the bone responds to mechanical force remains elusive. Here, we generated both orthodontic tooth movement (OTM) model in vivo and a cyclic stretch‐loading model in vitro to investigate biomechanical regulation of the alveolar bone. In this study, signal transducer and activator of transcription 3 (STAT3) was screened as one of the mechanosensitive proteins by protein array analysis of cyclic stretch‐loaded bone mesenchymal stem cells (BMSCs) and was also proven to be activated in osteoblasts in response to the mechanical force during OTM. With an inducible osteoblast linage‐specific Stat3 knockout model, we found that Stat3 deletion decelerated the OTM rate and reduced orthodontic force‐induced bone remodeling, as indicated by both decreased bone resorption and formation. Both genetic deletion and pharmacological inhibition of STAT3 in BMSCs directly inhibited mechanical force‐induced osteoblast differentiation and impaired osteoclast formation via osteoblast–osteoclast cross‐talk under mechanical force loading. According to RNA‐seq analysis of Stat3 ‐deleted BMSCs under mechanical force, matrix metalloproteinase 3 ( Mmp3) was screened and predicted to be a downstream target of STAT3 . The luciferase and ChIP assays identified that Stat3 could bind to the Mmp3 promotor and upregulate its transcription activity. Furthermore, STAT3‐inhibitor decelerated tooth movement through inhibition of the bone resorption activity, as well as MMP3 expression. In summary, our study identified the mechanosensitive characteristics of STAT3 in osteoblasts and highlighted its critical role in force‐induced bone remodeling during orthodontic tooth movement via osteoblast–osteoclast cross‐talk. © 2022 American Society for Bone and Mineral Research (ASBMR).
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    URL: Issue
    URL: Article
    DOI: 10.1002/jbmr.v38.1
    DOI: 10.1002/jbmr.4744
    RVK:
    XA 52230
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2008867-X
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  • 4
    Online Resource
    Online Resource
    Occlusal force orchestrates alveolar bone homeostasis via Piezo1 in female mice
    Oxford University Press (OUP) ; 2024
    In:  Journal of Bone and Mineral Research ( 2024-03-03)
    Details
    In: Journal of Bone and Mineral Research, Oxford University Press (OUP), ( 2024-03-03)
    Abstract: Healthy alveolar bone is the cornerstone of oral function and oral treatment. Alveolar bone is highly dynamic during the entire lifespan and is affected by both systemic and local factors. Importantly, alveolar bone is subjected to unique occlusal force in daily life, and mechanical force is a powerful trigger of bone remodeling, but the effect of occlusal force in maintaining alveolar bone mass remains ambiguous. In this study, the Piezo1 channel is identified as an occlusal force sensor. Activation of Piezo1 rescues alveolar bone loss caused by a loss of occlusal force. Moreover, we identify Piezo1 as the mediator of occlusal force in osteoblasts, maintaining alveolar bone homeostasis by directly promoting osteogenesis and by sequentially regulating catabolic metabolism through Fas ligand (FasL)-induced osteoclastic apoptosis. Interestingly, Piezo1 activation also exhibits remarkable efficacy in the treatment of alveolar bone osteoporosis caused by estrogen deficiency, which is highly prevalent among middle-aged and elderly women. Promisingly, Piezo1 may serve not only as a treatment target for occlusal force loss-induced alveolar bone loss but also as a potential target for metabolic bone loss, especially in older patients.
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    URL: Article
    DOI: 10.1093/jbmr/zjae032
    RVK:
    XA 52230
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2024
    detail.hit.zdb_id: 2008867-X
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