scholarly journals Endochondral ossification in hindlimbs during bufo gargarizans metamorphosis: A model of studying skeletal development in vertebrates

2018 ◽  
Vol 247 (10) ◽  
pp. 1121-1134 ◽  
Author(s):  
Jinshu Gao ◽  
Xinyi Li ◽  
Yuhui Zhang ◽  
Hongyuan Wang
Keyword(s):  
Endochondral Ossification ◽  
Skeletal Development ◽  
Bufo Gargarizans

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.

Loss of ephrinB1 in osteogenic progenitor cells impedes endochondral ossification and compromises bone strength integrity during skeletal development

Bone ◽  
2016 ◽  
Vol 93 ◽  
pp. 12-21 ◽  
Author(s):  
Thao M. Nguyen ◽  
Agnieszka Arthur ◽  
Sharon Paton ◽  
Sarah Hemming ◽  
Romana Panagopoulos ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Bone Strength ◽  
Endochondral Ossification ◽  
Skeletal Development

Identifying Candidate Mechanoregulators of Skeletal Development

2009 ◽  
Author(s):  
Niamh C. Nowlan ◽  
Patrick J. Prendergast ◽  
Shahragim Tajbakhsh ◽  
Paula Murphy
Keyword(s):  
Skeletal Muscle ◽  
Endochondral Ossification ◽  
Muscle Development ◽  
Skeletal Development ◽  
Endochondral Bone Formation ◽  
Mechanical Forces ◽  
Endochondral Bone ◽  
Mutant Strains ◽  
The Relationship

Studying the relationship between mechanical forces and skeletal development can provide vital clues to the mechanoregulation of skeletogenesis, providing important information to tissue engineers hoping to create functional cartilage or bone in vitro. Many studies of the mechanoregulation of skeletal development have focused on the chick embryo e.g., [1, 2]. However, as no endochondral ossification takes place in the embryonic chick long bones [1], mammalian systems must be used to examine the effect of mechanical forces on endochondral bone formation. Mouse mutant strains exist in which muscle development is affected, providing models with which to examine skeletogenesis in the absence of skeletal muscle contractions. One such strain is Pax3sp/sp [3], also known as splotch. The splotch mutant lacks the transcription factor Pax3, which prevents the migration of muscle pre-cursor cells into the limb buds, resulting in a complete absence of skeletal muscle.

scholarly journals Skeletal Malformations Caused by Overexpression of Cbfa1 or Its Dominant Negative Form in Chondrocytes

2001 ◽  
Vol 153 (1) ◽  
pp. 87-100 ◽  
Author(s):  
Chisato Ueta ◽  
Masahiro Iwamoto ◽  
Naoko Kanatani ◽  
Carolina Yoshida ◽  
Yang Liu ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Endochondral Ossification ◽  
Skeletal Development ◽  
Type Ii Collagen ◽  
Dominant Negative ◽  
Chondrocyte Maturation ◽  
Skeletal Malformations ◽  
Dominant Negative Form ◽  
Cellular Phenotypes

During skeletogenesis, cartilage develops to either permanent cartilage that persists through life or transient cartilage that is eventually replaced by bone. However, the mechanism by which cartilage phenotype is specified remains unclarified. Core binding factor α1 (Cbfa1) is an essential transcription factor for osteoblast differentiation and bone formation and has the ability to stimulate chondrocyte maturation in vitro. To understand the roles of Cbfa1 in chondrocytes during skeletal development, we generated transgenic mice that overexpress Cbfa1 or a dominant negative (DN)-Cbfa1 in chondrocytes under the control of a type II collagen promoter/enhancer. Both types of transgenic mice displayed dwarfism and skeletal malformations, which, however, resulted from opposite cellular phenotypes. Cbfa1 overexpression caused acceleration of endochondral ossification due to precocious chondrocyte maturation, whereas overexpression of DN-Cbfa1 suppressed maturation and delayed endochondral ossification. In addition, Cbfa1 transgenic mice failed to form most of their joints and permanent cartilage entered the endochondral pathway, whereas most chondrocytes in DN-Cbfa1 transgenic mice retained a marker for permanent cartilage. These data show that temporally and spatially regulated expression of Cbfa1 in chondrocytes is required for skeletogenesis, including formation of joints, permanent cartilages, and endochondral bones.

Altered temperature affect body condition and endochondral ossification in Bufo gargarizans tadpoles

2021 ◽  
pp. 103020
Author(s):  
Chaolu Ren ◽  
Yiran Teng ◽  
Yujia Shen ◽  
Qiong Yao ◽  
Hongyuan Wang
Keyword(s):  
Body Condition ◽  
Endochondral Ossification ◽  
Bufo Gargarizans

scholarly journals RECENT RESEARCH ON THE GROWTH PLATE: Advances in fibroblast growth factor signaling in growth plate development and disorders

2014 ◽  
Vol 53 (1) ◽  
pp. T11-T34 ◽  
Author(s):  
Yangli Xie ◽  
Siru Zhou ◽  
Hangang Chen ◽  
Xiaolan Du ◽  
Lin Chen
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Growth Plate ◽  
Endochondral Ossification ◽  
Molecular Mechanisms ◽  
Skeletal Development ◽  
Vital Role ◽  
Growth Factor Signaling ◽  
Missense Mutations ◽  
Fibroblast Growth

Skeletons are formed through two distinct developmental actions, intramembranous ossification and endochondral ossification. During embryonic development, most bone is formed by endochondral ossification. The growth plate is the developmental center for endochondral ossification. Multiple signaling pathways participate in the regulation of endochondral ossification. Fibroblast growth factor (FGF)/FGF receptor (FGFR) signaling has been found to play a vital role in the development and maintenance of growth plates. Missense mutations inFGFsandFGFRscan cause multiple genetic skeletal diseases with disordered endochondral ossification. Clarifying the molecular mechanisms of FGFs/FGFRs signaling in skeletal development and genetic skeletal diseases will have implications for the development of therapies for FGF-signaling-related skeletal dysplasias and growth plate injuries. In this review, we summarize the recent advances in elucidating the role of FGFs/FGFRs signaling in growth plate development, genetic skeletal disorders, and the promising therapies for those genetic skeletal diseases resulting from FGFs/FGFRs dysfunction. Finally, we also examine the potential important research in this field in the future.

scholarly journals Runx1 dose-dependently regulates endochondral ossification during skeletal development and fracture healing

2012 ◽  
Vol 27 (7) ◽  
pp. 1585-1597 ◽  
Author(s):  
Do Y Soung ◽  
Laleh Talebian ◽  
Christina J Matheny ◽  
Rosa Guzzo ◽  
Maren E Speck ◽  
...  
Keyword(s):  
Fracture Healing ◽  
Endochondral Ossification ◽  
Skeletal Development
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