Potential Involvement of Twist2 and Erk in the Regulation of Osteoblastogenesis by HB-EGF-EGFR Signaling

Nakamura, Takashi; Toita, Hidetoshi; Yoshimoto, A.; Nishimura, Daigo; Takagi, Tomoyo; Ogawa, Teiichiro; Takeya, Tatsuo; Ishida-Kitagawa, Norihiro

doi:10.1247/csf.10001

Cited by 29 publications

(35 citation statements)

References 25 publications

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“…Tenascin is synthesized by osteoblasts [35], and is able to stimulate osteoblastic differentiation through working with WNT signaling and BMP signaling [36]. Besides, parietal bone expressed higher levels of Msx2, Twist2, which are well-known transcriptional factor for osteoblast differentiation and bone formation [14, 37]. The higher levels of these genes expressions may account for osteoblast differentiation within parietal bone.…”

Section: Discussionmentioning

confidence: 99%

Physiological Signatures of Dual Embryonic Origins in Mouse Skull Vault

Zhao

et al. 2017

Cell Physiol Biochem

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Background/Aims: The mammalian skull vault is a highly regulated structure and consists of several membrane bones of different tissue origins (e.g. neural crest derived frontal bone and mesoderm derived parietal bone). Although membrane bones form through intramembranous ossification, neural crest derived frontal bone has superior osteoblast activity and bone regeneration ability, triggering a novel conception for craniofacial reconstruction and bone regeneration called endogenous calvarial regeneration. However, a comprehensive landscape of the genes and signaling pathways involved in this process is not clear. Methods: Transcriptome analysis within the two bone elements is firstly performed to determine the physiological signatures of differential gene expressions in mouse skull vault. Results: Frontal bone tissues and parietal bone tissues maintain tissue origin through special gene expression similar to neural crest vs mesoderm tissue, and physiological functions between these two tissues are also found in differences related to proliferation, differentiation and extracellular matrix production and clustered signaling pathways. Conclusion: Our data provide novel insights into the potential gene regulatory network in regulating the development of neural crest-derived frontal bone and mesoderm-derived parietal bone.

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Section: Discussionmentioning

confidence: 99%

Physiological Signatures of Dual Embryonic Origins in Mouse Skull Vault

Zhao

et al. 2017

Cell Physiol Biochem

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“…Subsequently, Ferron et al (65) demonstrated that insulin signaling in osteoblasts increased osteoclast activity and thereby the level of uncarboxylated osteocalcin, thus affecting glucose homeostasis. Fulzele et al reported that insulin promotes osteoblast development and osteocalcin expression and that bone formation and the number of osteoblasts were reduced in mice without insulin receptors in bone (181,182). With age, these mice developed adiposity and insulin resistance (181).…”

Section: Metabolic Aspects In Relation To a Homeostatic Model Involvimentioning

confidence: 99%

Genetics in Endocrinology: Autosomal dominant osteopetrosis revisited: lessons from recent studies

Bollerslev

Henriksen

Nielsen

et al. 2013

European Journal of Endocrinology

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Systematic studies of autosomal dominant osteopetrosis (ADO) were followed by the identification of underlying mutations giving unique possibilities to perform translational studies. What was previously designated ADO1 turned out to be a high bone mass phenotype caused by a missense mutation in the first propeller of LRP5, a region of importance for binding inhibitory proteins. Thereby, ADO1 cannot be regarded as a classical form of osteopetrosis but must now be considered a disease of LRP5 activation. ADO (Albers-Schönberg disease, or previously ADO2) is characterized by increased number of osteoclasts and a defect in the chloride transport system (ClC-7) of importance for acidification of the resorption lacuna (a form of Chloride Channel 7 Deficiency Osteopetrosis). Ex vivo studies of osteoclasts from ADO have shown that cells do form normally but have reduced resorption capacity and an expanded life span. Bone formation seems normal despite decreased osteoclast function. Uncoupling of formation from resorption makes ADO of interest for new strategies for treatment of osteoporosis. Recent studies have integrated bone metabolism in whole-body energy homeostasis. Patients with ADO may have decreased insulin levels indicating importance beyond bone metabolism. There seems to be a paradigm shift in the treatment of osteoporosis. Targeting ClC-7 might introduce a new principle of dual action. Drugs affecting ClC-7 could be antiresorptive, still allowing ongoing bone formation. Inversely, drugs affecting the inhibitory site of LRP5 might stimulate bone formation and inhibit resorption. Thereby, these studies have highlighted several intriguing treatment possibilities, employing novel modes of action, which could provide benefits to the treatment of osteoporosis.

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“…The medium was changed every 3 days. For ALP and Alizarin red staining, the detailed procedures were described previously [17].…”

Section: In Vitro Osteoblastogenesis and Cell Stainingmentioning

confidence: 99%

Osteogenic differentiation of C2C12 myogenic progenitor cells requires the Fos-related antigen Fra-1 – A novel target of Runx2

Geng

Sun³

et al. 2013

Biochemical and Biophysical Research Communications

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Potential Involvement of Twist2 and Erk in the Regulation of Osteoblastogenesis by HB-EGF-EGFR Signaling

Cited by 29 publications

References 25 publications

Physiological Signatures of Dual Embryonic Origins in Mouse Skull Vault

Physiological Signatures of Dual Embryonic Origins in Mouse Skull Vault

Genetics in Endocrinology: Autosomal dominant osteopetrosis revisited: lessons from recent studies

Osteogenic differentiation of C2C12 myogenic progenitor cells requires the Fos-related antigen Fra-1 – A novel target of Runx2

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