Role of perlecan in skeletal development and diseases

2002 ◽  
Vol 19 (4/5) ◽  
pp. 263-267 ◽  
Author(s):  
John Hassell ◽  
Yoshihiko Yamada ◽  
Eri Arikawa-Hirasawa
Keyword(s):  
Skeletal Development

scholarly journals Role of Thyroid Hormones in Skeletal Development and Bone Maintenance

2016 ◽  
Vol 37 (2) ◽  
pp. 135-187 ◽  
Author(s):  
J. H. Duncan Bassett ◽  
Graham R. Williams
Keyword(s):  
Thyroid Hormones ◽  
Skeletal Development ◽  
Bone Maintenance

scholarly journals Evolution and expansion of the RUNX2 QA repeat corresponds with the emergence of vertebrate complexity

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Axel H. Newton ◽  
Andrew J. Pask
Keyword(s):  
Natural Variation ◽  
Skeletal Development ◽  
Skull Shape ◽  
Morphological Novelty ◽  
Transactivation Potential ◽  
Repeat Domain ◽  
Related Transcription Factor ◽  
Mammalian Skull ◽  
Evolutionary Tuning

AbstractRunt-related transcription factor 2 (RUNX2) is critical for the development of the vertebrate bony skeleton. Unlike other RUNX family members, RUNX2 possesses a variable poly-glutamine, poly-alanine (QA) repeat domain. Natural variation within this repeat is able to alter the transactivation potential of RUNX2, acting as an evolutionary ‘tuning knob’ suggested to influence mammalian skull shape. However, the broader role of the RUNX2 QA repeat throughout vertebrate evolution is unknown. In this perspective, we examine the role of the RUNX2 QA repeat during skeletal development and discuss how its emergence and expansion may have facilitated the evolution of morphological novelty in vertebrates.

Role of the neural crest in development of the trabeculae and branchial arches in embryonic sea lamprey, Petromyzon marinus (L)

Development ◽  
1988 ◽  
Vol 102 (2) ◽  
pp. 301-310 ◽  
Author(s):  
R.M. Langille ◽  
B.K. Hall
Keyword(s):  
Neural Crest ◽  
Skeletal Development ◽  
Petromyzon Marinus ◽  
Branchial Arches ◽  
Artificial Fertilization ◽  
Vertebrate Skeleton ◽  
The Brain ◽  
Head Skeleton ◽  
Neurula Stage

Lamprey embryos were obtained by artificial fertilization to ascertain the contributions made by the neural crest to the head skeleton. Early-neurula-stage embryos of Petromyzon marinus were subjected to neural crest extirpation along the anterior half from one of seven zones, raised to a larval stage at which control larvae exhibit well-developed skeletons and analysed by light microscopy for any abnormalities to the cranial and visceral skeleton. The removal of premigratory neural crest at the level of the anterior prosencephalon (zone I) and at the level of somites 6 to 8 (zone VII) had no effect on skeletal development. However, the extirpation of neural crest from the intervening regions was positively correlated with deletions/reductions to the trabeculae (basicranial elements) and to the branchial arches (viscerocranial elements). Alterations to the trabeculae (16/27 cases, or 59%) occurred only after extirpation of zones II-V (corresponding to the posterior prosencephalon to midrhombencephalon) while alterations to the branchial arches (21/28 cases, or 75%) occurred only after removal of neural crest from zones III-VI (corresponding to the mesencephalon to the level of the fifth somite). Furthermore, the first three branchial arches were correlated in a majority of cases with neural crest from zone III, the next two arches with zones IV, V and VI and the last two arches with zone VI. Organs that develop within or adjacent to the area of neural crest extirpation such as the brain, notochord and lateral mesodermal derivatives were not affected. Parachordals were never altered by the operations nor were there any discernible changes to developing mucocartilage or to the prechondrogenic otic capsule. The contributions of the neural crest to the petromyzonid head skeleton described herein are compared with the roles of neural crest in the development of cranial and visceral skeletal elements in other vertebrates. The importance of these findings to the current hypothesis of the phylogeny of the vertebrate skeleton and the central role of the neural crest in vertebrate cephalization is discussed.

The Influence of the Dietary Protein Content on Growth in Giant Breed Dogs

1993 ◽  
Vol 06 (01) ◽  
pp. 01-08 ◽  
Author(s):  
H. A. W. Hazewinkel ◽  
G. Voorhout ◽  
W. J. Biewenga ◽  
J. P. Koeman ◽  
S. A. Goedegebuure ◽  
...  
Keyword(s):  
Protein Content ◽  
Dietary Protein ◽  
Skeletal Development ◽  
Causative Role ◽  
Plasma Albumin ◽  
Plasma Urea ◽  
Enchondral Ossification ◽  
Per Se ◽  
Great Dane

SummaryFeeding immature dogs of large breeds a diet exceeding the NRC recommendations (5) for energy, protein, calcium (Ca), phosphorus (P), and vitamin D may result in disturbances of skeletal development. The effects of excess energy and various Ca:P ratios per se have been reported. The role of dietary protein, especially with regard to skeletal growth in giantbreed dogs was studied. Clinical, biochemical, radiographical, and histological parameters were studied in three groups of Great Dane pups raised on diets only differing in protein content (14.6, 23.1 and 31.6% dm respectively). Significant differences were found for body weight, plasma albumin, and plasma urea. The differences in protein intake per se had no demonstrable consequences for renal and skeletal development. A causative role for dietary protein in disturbed enchondral ossification in dogs is unlikely.Nutrition is important during growth, especially in giant breed dogs. The role of dietary protein with regard to skeletal development was studied in three groups of Great Dane pups raised on diets only differing in protein content. A causative role for dietary protein in disturbed enchondral ossification is unlikely.

Role of FGFs/FGFRs in skeletal development and bone regeneration

2012 ◽  
Vol 227 (12) ◽  
pp. 3731-3743 ◽  
Author(s):  
Xiaolan Du ◽  
Yangli Xie ◽  
Cory J. Xian ◽  
Lin Chen
Keyword(s):  
Bone Regeneration ◽  
Skeletal Development

scholarly journals Stage-Specific Secretion of HMGB1 in Cartilage Regulates Endochondral Ossification

2007 ◽  
Vol 27 (16) ◽  
pp. 5650-5663 ◽  
Author(s):  
Noboru Taniguchi ◽  
Kenji Yoshida ◽  
Tatsuo Ito ◽  
Masanao Tsuda ◽  
Yasunori Mishima ◽  
...  
Keyword(s):  
Endochondral Ossification ◽  
Skeletal Development ◽  
High Mobility ◽  
Immunohistochemical Analysis ◽  
Dual Function ◽  
Hmgb1 Protein ◽  
Tissue Organization ◽  
Extracellular Release ◽  
Extracellular Factor

ABSTRACT High mobility group box 1 protein (HMGB1) is a chromatin protein that has a dual function as a nuclear factor and as an extracellular factor. Extracellular HMGB1 released by damaged cells acts as a chemoattractant, as well as a proinflammatory cytokine, suggesting that HMGB1 is tightly connected to the process of tissue organization. However, the role of HMGB1 in bone and cartilage that undergo remodeling during embryogenesis, tissue repair, and disease is largely unknown. We show here that the stage-specific secretion of HMGB1 in cartilage regulates endochondral ossification. We analyzed the skeletal development of Hmgb1 −/− mice during embryogenesis and found that endochondral ossification is significantly impaired due to the delay of cartilage invasion by osteoclasts, osteoblasts, and blood vessels. Immunohistochemical analysis revealed that HMGB1 protein accumulated in the cytosol of hypertrophic chondrocytes at growth plates, and its extracellular release from the chondrocytes was verified by organ culture. Furthermore, we demonstrated that the chondrocyte-secreted HMGB1 functions as a chemoattractant for osteoclasts and osteoblasts, as well as for endothelial cells, further supporting the conclusion that Hmgb1 −/− mice are defective in cell invasion. Collectively, these findings suggest that HMGB1 released from differentiating chondrocytes acts, at least in part, as a regulator of endochondral ossification during osteogenesis.

scholarly journals Role of Cartilage-Associated Protein in Skeletal Development

2010 ◽  
Vol 8 (2) ◽  
pp. 77-83 ◽  
Author(s):  
Roy Morello ◽  
Frank Rauch
Keyword(s):  
Skeletal Development

scholarly journals Mice Lacking the Calcineurin Inhibitor Rcan2 Have an Isolated Defect of Osteoblast Function

Endocrinology ◽  
2012 ◽  
Vol 153 (7) ◽  
pp. 3537-3548 ◽  
Author(s):  
J. H. Duncan Bassett ◽  
John G. Logan ◽  
Alan Boyde ◽  
Moira S. Cheung ◽  
Holly Evans ◽  
...  
Keyword(s):  
T Cells ◽  
Bone Development ◽  
Skeletal Development ◽  
Dominant Negative ◽  
Nuclear Factor ◽  
Activated T Cells ◽  
Osteoblast Function ◽  
And Function

Calcineurin-nuclear factor of activated T cells signaling controls the differentiation and function of osteoclasts and osteoblasts, and regulator of calcineurin-2 (Rcan2) is a physiological inhibitor of this pathway. Rcan2 expression is regulated by T3, which also has a central role in skeletal development and bone turnover. To investigate the role of Rcan2 in bone development and maintenance, we characterized Rcan2−/− mice and determined its skeletal expression in T3 receptor (TR) knockout and thyroid-manipulated mice. Rcan2−/− mice had normal linear growth but displayed delayed intramembranous ossification, impaired cortical bone formation, and reduced bone mineral accrual during development as well as increased mineralization of adult bone. These abnormalities resulted from an isolated defect in osteoblast function and are similar to skeletal phenotypes of mice lacking the type 2 deiodinase thyroid hormone activating enzyme or with dominant-negative mutations of TRα, the predominant TR isoform in bone. Rcan2 mRNA was expressed in primary osteoclasts and osteoblasts, and its expression in bone was differentially regulated in TRα and TRβ knockout and thyroid-manipulated mice. However, in primary osteoblast cultures, T3 treatment did not affect Rcan2 mRNA expression or nuclear factor of activated T cells c1 expression and phosphorylation. Overall, these studies establish that Rcan2 regulates osteoblast function and its expression in bone is regulated by thyroid status in vivo.

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