Recombinant mouse periostin ameliorates coronal sutures fusion in Twist1+/− mice

Bai, Shanshan; Li, Dong; Xu, Liang; Duan, Huanan; Yuan, Jie; Wei, Min

doi:10.1186/s12967-018-1454-2

Cited by 7 publications

(7 citation statements)

References 41 publications

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“…Integrin αvβ3 is directly involved in the downregulation of sclerostin induced by POSTN (Tu et al 2012). In recent studies, POSTN, induced by estrogen, could mediate the osteogenic differentiation of bone marrow stromal cells in ovariectomized rats (Li et al 2020), could promote the osteogenesis of CTLA4‐modified human bone marrow mesenchymal stem cells (Zhang et al 2017b), and could promote coronal suture fusion in Twist 1± mice (Bai et al 2018). These processes cannot be separated from the classical Wnt/β‐catenin pathway.…”

Section: Postn and The Wnt Pathwaymentioning

confidence: 99%

Periostin: an emerging activator of multiple signaling pathways

Wang

Zhu

et al. 2022

J. Cell Commun. Signal.

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Matricellular proteins are responsible for regulating the microenvironment, the behaviors of surrounding cells, and the homeostasis of tissues. Periostin (POSTN), a non‐structural matricellular protein, can bind to many extracellular matrix proteins through its different domains. POSTN usually presents at low levels in most adult tissues but is highly expressed in pathological sites such as in tumors and inflamed organs. POSTN can bind to diverse integrins to interact with multiple signaling pathways within cells, which is one of its core biological functions. Increasing evidence shows that POSTN can activate the TGF‐β, the PI3K/Akt, the Wnt, the RhoA/ROCK, the NF‐κB, the MAPK and the JAK pathways to promote the occurrence and development of many diseases, especially cancer and inflammatory diseases. Furthermore, POSTN can interact with some pathways in an upstream and downstream relationship, forming complicated crosstalk. This article focuses on the interactions between POSTN and different signaling pathways in diverse diseases, attempting to explain the mechanisms of interaction and provide novel guidelines for the development of targeted therapies.

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Section: Postn and The Wnt Pathwaymentioning

confidence: 99%

Periostin: an emerging activator of multiple signaling pathways

Wang

Zhu

et al. 2022

J. Cell Commun. Signal.

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“…Recombinant periostin, an extracellular matrix protein, is also reported to mitigate coronal craniosynostosis in Twist1 +/− mice ( Bai et al, 2018 ). Periostin is expressed in mesenchymal cells in the mouse skull and is repressed by Twist1.…”

Section: Prospective Treatments For Craniosynostosismentioning

confidence: 99%

The clinical manifestations, molecular mechanisms and treatment of craniosynostosis

Stanton

Urata

Chen

et al. 2022

Disease Models &Amp; Mechanisms

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Craniosynostosis is a major congenital craniofacial disorder characterized by the premature fusion of cranial suture(s). Patients with severe craniosynostosis often have impairments in hearing, vision, intracranial pressure and/or neurocognitive functions. Craniosynostosis can result from mutations, chromosomal abnormalities or adverse environmental effects, and can occur in isolation or in association with numerous syndromes. To date, surgical correction remains the primary treatment for craniosynostosis, but it is associated with complications and with the potential for re-synostosis. There is, therefore, a strong unmet need for new therapies. Here, we provide a comprehensive review of our current understanding of craniosynostosis, including typical craniosynostosis types, their clinical manifestations, cranial suture development, and genetic and environmental causes. Based on studies from animal models, we present a framework for understanding the pathogenesis of craniosynostosis, with an emphasis on the loss of postnatal suture mesenchymal stem cells as an emerging disease-driving mechanism. We evaluate emerging treatment options and highlight the potential of mesenchymal stem cell-based suture regeneration as a therapeutic approach for craniosynostosis.

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“…Several studies of deregulated pathways caused by mutations underlying craniosynostosis have provided promising compounds in designing non-invasive adjuvant treatments for CS patients. On this regard, Bai and colleagues showed that recombinant mouse periostin can reduce proliferation, migration and osteogenic differentiation of suture-derived cells, as well as can decrease coronal suture fusion in Twist1 +/− mice model of Saethre-Chotzen syndrome, restoring the loss of TWIST1 due to haploinsufficiency [134]. Other approaches have evaluated the feasibility of pharmacological therapies acting through interference or downregulation of FGF/FGFR2 and Wnt signalling at the suture interface.…”

Section: Bioactive Compounds and Delivery Systemsmentioning

confidence: 99%

Personalized Bone Reconstruction and Regeneration in the Treatment of Craniosynostosis

et al. 2021

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Craniosynostosis (CS) is the second most prevalent craniofacial congenital malformation due to the premature fusion of skull sutures. CS care requires surgical treatment of variable complexity, aimed at resolving functional and cosmetic defects resulting from the skull growth constrain. Despite significant innovation in the management of CS, morbidity and mortality still exist. Residual cranial defects represent a potential complication and needdedicated management to drive a targeted bone regeneration while modulating suture ossification. To this aim, existing techniques are rapidly evolving and include the implementation of novel biomaterials, 3D printing and additive manufacturing techniques, and advanced therapies based on tissue engineering. This review aims at providing an exhaustive and up-to-date overview of the strategies in use to correct these congenital defects, focusing on the technological advances in the fields of biomaterials and tissue engineering implemented in pediatric surgical skull reconstruction, i.e., biodegradable bone fixation systems, biomimetic scaffolds, drug delivery systems, and cell-based approaches.

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Recombinant mouse periostin ameliorates coronal sutures fusion in Twist1+/− mice

Cited by 7 publications

References 41 publications

Periostin: an emerging activator of multiple signaling pathways

Periostin: an emerging activator of multiple signaling pathways

The clinical manifestations, molecular mechanisms and treatment of craniosynostosis

Personalized Bone Reconstruction and Regeneration in the Treatment of Craniosynostosis

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