Exogenous FGF8 signaling in osteocytes leads to mandibular hypoplasia in mice

Xu, Jue; Wang, Linyan; Huang, Zhen; Shao, Meiying

doi:10.1111/odi.13262

Cited by 4 publications

(3 citation statements)

References 22 publications

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“…FGF signaling contributes to the development of most craniofacial structures, such as the development and outgrowth of the facial primordia, craniofacial skeletogenesis, palatogenesis, as well as development of submandibular salivary gland, teeth, eye lids, craniofacial muscles, and muscular tongue ( Nie et al, 2006 ; Prochazkova et al, 2018 ; Weng et al, 2018 ). Perturbation of FGF signaling is involved in various craniofacial abnormalities, including facial or palatal cleft, midface agenesis, mandibular hypoplasia, open eyelids at an early postnatal stage, and craniosynostosis ( Ibrahimi et al, 2004 ; Rice et al, 2004 ; Wang et al, 2013 ; Prochazkova et al, 2018 ; Ray et al, 2020 ; Xu et al, 2020 ).…”

Section: Fgf Signalingmentioning

confidence: 99%

FGF signaling in cranial suture development and related diseases

Zhao

Erhardt

Sung

et al. 2023

Front. Cell Dev. Biol.

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Suture mesenchymal stem cells (SMSCs) are a heterogeneous stem cell population with the ability to self-renew and differentiate into multiple cell lineages. The cranial suture provides a niche for SMSCs to maintain suture patency, allowing for cranial bone repair and regeneration. In addition, the cranial suture functions as an intramembranous bone growth site during craniofacial bone development. Defects in suture development have been implicated in various congenital diseases, such as sutural agenesis and craniosynostosis. However, it remains largely unknown how intricate signaling pathways orchestrate suture and SMSC function in craniofacial bone development, homeostasis, repair and diseases. Studies in patients with syndromic craniosynostosis identified fibroblast growth factor (FGF) signaling as an important signaling pathway that regulates cranial vault development. A series of in vitro and in vivo studies have since revealed the critical roles of FGF signaling in SMSCs, cranial suture and cranial skeleton development, and the pathogenesis of related diseases. Here, we summarize the characteristics of cranial sutures and SMSCs, and the important functions of the FGF signaling pathway in SMSC and cranial suture development as well as diseases caused by suture dysfunction. We also discuss emerging current and future studies of signaling regulation in SMSCs.

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Section: Fgf Signalingmentioning

confidence: 99%

FGF signaling in cranial suture development and related diseases

Zhao

Erhardt

Sung

et al. 2023

Front. Cell Dev. Biol.

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“…When FGF‐8 interacts with an FGFR3 mutant, ectopic cartilage and osteophytes are generated, resulting in Kashin‐Beck disease or abnormal cartilage and bone 68,69 . Simultaneously, overexpression of FGF‐8 in combination with FGFR causes abnormal cartilage proliferation and promotes a cartilage fate in normal tissues rather than osteogenesis 70,71 . Based on these findings, FGF‐8 and FGFR should exert a negative regulatory effect on the proliferation and differentiation of chondrocytes in normal cartilage tissue.…”

Section: Overview Of Fgf‐8 In Normal Cartilagementioning

confidence: 99%

The role of fibroblast growth factor 8 in cartilage development and disease

Chen

Cui

Zhang

et al. 2022

J Cellular Molecular Medi

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Fibroblast growth factor 8 (FGF‐8), also known as androgen‐induced growth factor (AIGF), is presumed to be a potent mitogenic cytokine that plays important roles in early embryonic development, brain formation and limb development. In the bone environment, FGF‐8 produced or received by chondrocyte precursor cells binds to fibroblast growth factor receptor (FGFR), causing different levels of activation of downstream signalling pathways, such as phospholipase C gamma (PLCγ)/Ca2+, RAS/mitogen‐activated protein kinase‐extracellular regulated protein kinases (RAS/MAPK‐MEK‐ERK), and Wnt‐β‐catenin‐Axin2 signalling, and ultimately controlling chondrocyte proliferation, differentiation, cell survival and migration. However, the molecular mechanism of FGF‐8 in normal or pathological cartilage remains unclear, and thus, FGF‐8 represents a novel exploratory target for studies of chondrocyte development and cartilage disease progression. In this review, studies assessing the relationship between FGF‐8 and chondrocytes that have been published in the past 5 years are systematically summarized to determine the probable mechanism and physiological effect of FGF‐8 on chondrocytes. Based on the existing research results, a therapeutic regimen targeting FGF‐8 is proposed to explore the possibility of treating chondrocyte‐related diseases.

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“…But the Osr2 -Cre is limited to study the palatogenesis and pattern formation during palate development because of the specific expression of Osr2 in palatal shelves. Dmp1 -Cre is also an allele that can be used in the craniofacial region; however, the Dmp1 + cells were restricted in osteocytes in maxilla-mandibular regions 14 , 15 . Osx -Cre mice is another strain that has been used for studying the mechanisms of both bone and dental mesenchymal tissue 16 , 17 .…”

Section: Introductionmentioning

confidence: 99%

The effects of altered BMP4 signaling in first branchial-arch-derived murine embryonic orofacial tissues

Chen

Yan

et al. 2021

Int J Oral Sci

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The first branchial arch (BA1), which is derived from cranial neural crest (CNC) cells, gives rise to various orofacial tissues. Cre mice are widely used for the determination of CNC and exploration of gene functions in orofacial development. However, there is a lack of Cre mice specifically marked BA1’s cells. Pax2-Cre allele was previously generated and has been widely used in the field of inner ear development. Here, by compounding Pax2-Cre and R26R-mTmG mice, we found a specific expression pattern of Pax2+ cells that marked BA1’s mesenchymal cells and the BA1-derivatives. Compared to Pax2-Cre; R26R-mTmG allele, GFP+ cells were abundantly found both in BA1 and second branchial arch in Wnt1-Cre;R26R-mTmG mice. As BMP4 signaling is required for orofacial development, we over-activated Bmp4 by using Pax2-Cre; pMes-BMP4 strain. Interestingly, our results showed bilateral hyperplasia between the upper and lower teeth. We also compare the phenotypes of Wnt1-Cre; pMes-BMP4 and Pax2-Cre; pMes-BMP4 strains and found severe deformation of molar buds, palate, and maxilla-mandibular bony structures in Wnt1-Cre; pMes-BMP4 mice; however, the morphology of these orofacial organs were comparable between controls and Pax2-Cre; pMes-BMP4 mice except for bilateral hyperplastic tissues. We further explore the properties of the hyperplastic tissue and found it is not derived from Runx2+ cells but expresses Msx1, and probably caused by abnormal cell proliferation and altered expression pattern of p-Smad1/5/8. In sum, our findings suggest altering BMP4 signaling in BA1-specific cell lineage may lead to unique phenotypes in orofacial regions, further hinting that Pax2-Cre mice could be a new model for genetic manipulation of BA1-derived organogenesis in the orofacial region.

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Exogenous FGF8 signaling in osteocytes leads to mandibular hypoplasia in mice

Cited by 4 publications

References 22 publications

FGF signaling in cranial suture development and related diseases

FGF signaling in cranial suture development and related diseases

The role of fibroblast growth factor 8 in cartilage development and disease

The effects of altered BMP4 signaling in first branchial-arch-derived murine embryonic orofacial tissues

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