Expression and function of BMP3 during chick limb development

Gamer, Laura W.; Ho, Victoria M.; Cox, Karen; Rosen, Vicki

doi:10.1002/dvdy.21561

Cited by 34 publications

(29 citation statements)

References 27 publications

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“…It is likely that the perichondrium negatively regulates chondrocyte maturation through more than one mechanism and this may include BMP3 controlling signaling through ActRIIB. The phenotype we observed in the BMP3 transgenic mice is similar to that seen in BMP3 infected chick limbs where expanded zones of hypertrophic chondrocytes and altered perichondrial formation also occur (Gamer et al, 2008). Taken together, these data suggest that the periosteum and the perichondrium and its adjacent chondrocytes are important targets for BMP3 action.…”

Section: Discussionsupporting

confidence: 72%

Overexpression of BMP3 in the developing skeleton alters endochondral bone formation resulting in spontaneous rib fractures

Gamer

Cox

Carlo

et al. 2009

Developmental Dynamics

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Bone morphogenetic protein-3 (BMP) has been identified as a negative regulator in the skeleton as mice lacking BMP3 have increased bone mass. To further understand how BMP3 mediates bone formation, we created transgenic mice overexpressing BMP3 using the type I collagen promoter. BMP3 transgenic mice displayed spontaneous rib fractures that were first detected at E17.0. The fractures were due to defects in differentiation of the periosteum and late hypertrophic chondrocytes resulting in thinner cortical bone with decreased mineralization. As BMP3 modulates BMP and activin signaling through ActRIIB, we examined the ribs of ActRIIB receptor knockout mice and found they had defects in late chondrogenesis and mineralization similar to BMP3 transgenic mice. These data suggest that BMP3 exerts its effects in the skeleton by altering signaling through ActRIIB in chondrocytes and the periosteum, and this results in defects in bone collar formation and late hypertrophic chondrocyte maturation leading to decreased mineralization and less bone.

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Section: Discussionsupporting

confidence: 72%

Overexpression of BMP3 in the developing skeleton alters endochondral bone formation resulting in spontaneous rib fractures

Gamer

Cox

Carlo

et al. 2009

Developmental Dynamics

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“…The BMP-3 molecule demonstrates high affinity to the activin receptor ActRII, but lower to ActRIIb. Next, the signal is carried to the cell nucleus using the SMAD protein [27]. Expression is located mainly in the neuroectodermis and the forming s periosteum, which suggests that BMP-3 may be engaged in www.journals.viamedica.pl [25], own modified.…”

Section: The Bmp Protein and Bmpr Receptor: Expression Function And mentioning

confidence: 99%

Selected Bone Morphogenetic Proteins—The Possibility of Their Use in the Diagnostics and Therapy of Severe Asthma

Koćwin

Jonakowski

Przemęcka

et al. 2017

Advances in Respiratory Medicine

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Asthma is a chronic heterogeneous illness of the lower airway with an inflammatory basis, developing from hyperresponsiveness and bronchial obstruction. One of the more unfavourable processes occurring in the airway are the long-term changes of the respiratory tract known as remodelling, resulting in complete irreversible obstruction. Bone morphogenetic protein (BMP) is a member of the Transforming Growth Factor beta (TGF-b) superfamily, which regulates processes in embryonic and post-embryonic development. The role played by BMP is regulation of degradation and remodelling of the extracellular matrix, which is one of the elements involved in the reconstruction of the structure of the bronchi in severe asthma. This paper presents the antagonistic properties of BMP against TGF-b, anti-inflammatory and counteracting fibrosis in the respiratory tract. The current state of knowledge indicates that this group of cytokines are potential new markers of remodelling in severe asthma, and further studies on their therapeutic value are necessary.

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“…Among the local signaling pathways that are known to play a role in these processes are the canonical Wnt signaling (Akiyama et al, 2004; Hartmann, 2006; Hartmann and Tabin, 2000; Hu et al, 2005; Kawakami et al, 2000; Kawakami et al, 1999; Krishnan et al, 2006; Westendorf et al, 2004; Yamaguchi et al, 1999), bone morphogenetic protein (BMP) (Canalis et al, 2003; Ducy and Karsenty, 2000; Hoffmann and Gross, 2001; Kronenberg, 2003), parathyroid hormone related peptide (PTHrP), Indian Hedgehog (Ihh) (Chung et al, 1998; Chung et al, 2001; Karaplis et al, 1994; Karp et al, 2000; Kobayashi et al, 2002; Kronenberg, 2003; Lanske et al, 1999; Schipani et al, 1997; St-Jacques et al, 1999; Vortkamp et al, 1996) and fibroblast growth factor (FGF) (Colvin et al, 1996; Kronenberg, 2003; Marie, 2003; Ornitz, 2005; Wang et al, 1999) pathways. Several studies have demonstrated that the perichondrium regulates cartilage growth, by providing a source of signaling molecules that regulate chondrocyte proliferation and differentiation (Di Nino et al, 2001; Gamer et al, 2008; Hinoi et al, 2006; Long and Linsenmayer, 1998; Marie, 2003; Ornitz, 2005; Vortkamp et al, 1996). …”

Section: Introductionmentioning

confidence: 99%

Perichondrial expression of Wdr5 regulates chondrocyte proliferation and differentiation

Gori

Zhu

Demay

2009

Developmental Biology

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Wdr5 is developmentally expressed in osteoblasts and is required for osteoblast differentiation. Mice overexpressing Wdr5 under the control of the mouse α(1)I collagen promoter (Col I-Wdr5) display accelerated osteoblast differentiation as well as accelerated chondrocyte differentiation, suggesting that overexpression of Wdr5 in osteoblasts affects chondrocyte differentiation. To elucidate the molecular mechanism by which overexpression of Wdr5 in the perichondrium regulates chondrocyte differentiation, studies were undertaken using skeletal elements and cultured metatarsals isolated from wild-type and Col I-Wdr5 embryos. FGF18 mRNA levels were decreased in Col I-Wdr5 humeri. Furthermore, local delivery of FGF18 to the bone collar of ex vivo cultures of metatarsals attenuated the chondrocyte phenotype of the Col I-Wdr5 metatarsals. Impairing local FGF action in wild-type metatarsals resulted in a chondrocyte phenotype analogous to that of Col I-Wdr5 metatarsals implicating impaired FGF action as the cause of the phenotype observed. The expression of Twist-1, which regulates chondrocyte differentiation, was increased in Col I-Wdr5 humeri. Chromatin immunoprecipitation analyses demonstrated that Wdr5 is recruited to the Twist-1 promoter. These findings support a model in which overexpression of Wdr5 in the perichondrium promotes chondrocyte differentiation by modulating the expression of Twist-1 and FGF18.

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Expression and function of BMP3 during chick limb development

Cited by 34 publications

References 27 publications

Overexpression of BMP3 in the developing skeleton alters endochondral bone formation resulting in spontaneous rib fractures

Overexpression of BMP3 in the developing skeleton alters endochondral bone formation resulting in spontaneous rib fractures

Selected Bone Morphogenetic Proteins—The Possibility of Their Use in the Diagnostics and Therapy of Severe Asthma

Perichondrial expression of Wdr5 regulates chondrocyte proliferation and differentiation

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