Critical roles of the TGF-β type I receptor ALK5 in perichondrial formation and function, cartilage integrity, and osteoblast differentiation during growth plate development

Matsunobu, Tomoya; Torigoe, Kiyoyuki; Ishikawa, Mayuko; Vega, Susana de; Kulkarni, Ashok B.; Iwamoto, Yukihide; Yamada, Yoshihiko

doi:10.1016/j.ydbio.2009.06.002

Cited by 110 publications

(98 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…S1B). TGF␤ signaling is reported to be involved in the proliferation of perichondrial cells and osteoblast differentiation (26,27). In the cultured metatarsals in the present study, rhTGF␤1 increased the thickness of the perichondrium and inhibited the SAG-induced ectopic bone collar formation (supplemental.…”

Section: Development Of An Organ Culture System That Enables the Obsesupporting

confidence: 52%

Hedgehog-Gli Activators Direct Osteo-chondrogenic Function of Bone Morphogenetic Protein toward Osteogenesis in the Perichondrium

Hojo

Ohba

Taniguchi

et al. 2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: During endochondral ossification, cells in the perichondrium give rise to osteoblast precursors. Results: Bone morphogenetic protein (BMP) interacted with hedgehog (Hh) to enhance osteogenesis, whereas in the absence of Hh, BMP enhanced ectopic chondrogenesis in the perichondrium. Conclusion: Hh alters the function of BMP to specify perichondrial cells into osteoblasts.Significance: This provides an insight into signaling network in osteogenesis.

show abstract

Section: Development Of An Organ Culture System That Enables the Obsesupporting

confidence: 52%

Hedgehog-Gli Activators Direct Osteo-chondrogenic Function of Bone Morphogenetic Protein toward Osteogenesis in the Perichondrium

Hojo

Ohba

Taniguchi

et al. 2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Mesenchymal Mek mutation caused kyphosis and omphalocele, mimicking human pathological conditions that can impose a significant physical restriction on lung growth and function (Argyle, 1989;McMaster et al, 2007). In addition to Fgfr1;Fgfr2 compound mutants, abnormal body wall formation was seen in mice carrying conditional mutations in the Alk3 gene encoding a BMP type I receptor, and the Alk5 gene encoding a Tgfβ type I receptor (Matsunobu et al, 2009;Sun et al, 2007). BMP4 and TGFβ were shown to activate the ERK/MAPK pathway in various experimental conditions (Hough et al, 2012;Lee et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Crucial requirement of ERK/MAPK signaling in respiratory tract development

et al. 2014

View full text Add to dashboard Cite

There was an error published in Development 141, 3197-3211.In the key for Fig. 3C, the grey bars were labelled with the incorrect genotype name. The correct genotype is Mek1 +/flox ;Mek2+/cre . This error does not affect the conclusions of the paper.The authors apologise to readers for this mistake. In vitro, the loss of Mek function in lung mesenchyme did not interfere with lung growth and branching, suggesting that both the reduced intrathoracic space due to the dysmorphic rib cage and the omphalocele impaired lung development in vivo. Conversely, Mek mutation in the respiratory epithelium caused lung agenesis, a phenotype resulting from the direct impact of the ERK/MAPK pathway on cell proliferation and survival. No tracheal epithelial cell differentiation occurred and no SOX2-positive progenitor cells were detected in mutants, implying a role for the ERK/MAPK pathway in trachea progenitor cell maintenance and differentiation. Moreover, these anomalies were phenocopied when the Erk1 and Erk2 genes were mutated in airway epithelium. Thus, the ERK/MAPK pathway is required for the integration of mesenchymal and epithelial signals essential for the development of the entire respiratory tract.

show abstract

“…TGFb signaling controls longitudinal bone growth through inhibition of chondrocyte terminal differentiation and maintenance of the proliferating chondrocyte pool (Serra et al 1997;Alvarez et al 2001;Yang et al 2001;Alvarez and Serra 2004). Consequently, conditional inactivation of Tgfbr2 or Tgfbr1, which leads to ablation of TGF-b signaling, results in severe shortening of the limbs among other skeletal manifestations (Baffi et al 2004;Seo and Serra 2007;Matsunobu et al 2009;Hiramatsu et al 2011). …”

Section: Regulation Of Chondrogenesis and Longitudinal Bone Growth Bymentioning

confidence: 99%

TGF-β Family Signaling in Connective Tissue and Skeletal Diseases

MacFarlane

Haupt

Dietz

et al. 2017

Cold Spring Harb Perspect Biol

View full text Add to dashboard Cite

The transforming growth factor b (TGF-b) family of signaling molecules, which includes TGF-bs, activins, inhibins, and numerous bone morphogenetic proteins (BMPs) and growth and differentiation factors (GDFs), has important functions in all cells and tissues, including soft connective tissues and the skeleton. Specific TGF-b family members play different roles in these tissues, and their activities are often balanced with those of other TGF-b family members and by interactions with other signaling pathways. Perturbations in TGF-b family pathways are associated with numerous human diseases with prominent involvement of the skeletal and cardiovascular systems. This review focuses on the role of this family of signaling molecules in the pathologies of connective tissues that manifest in rare genetic syndromes (e.g., syndromic presentations of thoracic aortic aneurysm), as well as in more common disorders (e.g., osteoarthritis and osteoporosis). Many of these diseases are caused by or result in pathological alterations of the complex relationship between the TGF-b family of signaling mediators and the extracellular matrix in connective tissues.T he transforming growth factor b (TGF-b) family of cytokines comprises the three TGF-b proteins (TGF-b1, TGF-b2, and TGFb3) and related growth and differentiation factors such as activins, inhibins, bone morphogenic proteins (BMPs), and growth and differentiation factors (GDFs). These molecules play critical roles both in normal development and in several pathological conditions, including inflammation, fibrosis, and cancer (reviewed in Li and Flavell 2006;Gordon and Blobe 2008;Ikushima and Miyazono 2010). This review focuses on the role of these proteins in development and homeostasis of the skeleton and other connective tissues (summarized in Fig. 1) and on the diseases that ensue when these pathways are altered. Aberrant signaling in these pathways has been associated with common connective 6 These authors contributed equally to this work.

show abstract

Critical roles of the TGF-β type I receptor ALK5 in perichondrial formation and function, cartilage integrity, and osteoblast differentiation during growth plate development

Cited by 110 publications

References 57 publications

Hedgehog-Gli Activators Direct Osteo-chondrogenic Function of Bone Morphogenetic Protein toward Osteogenesis in the Perichondrium

Hedgehog-Gli Activators Direct Osteo-chondrogenic Function of Bone Morphogenetic Protein toward Osteogenesis in the Perichondrium

Crucial requirement of ERK/MAPK signaling in respiratory tract development

TGF-β Family Signaling in Connective Tissue and Skeletal Diseases

Contact Info

Product

Resources

About