Faculty Opinions recommendation of Studies on the role of Dlx5 in regulation of chondrocyte differentiation during endochondral ossification in the developing mouse limb.

2011 ◽  
Author(s):  
Pancras Hogendoorn ◽  
Judith Bovee
Keyword(s):  
Endochondral Ossification ◽  
Chondrocyte Differentiation ◽  
Mouse Limb

scholarly journals Studies on the role of Dlx5 in regulation of chondrocyte differentiation during endochondral ossification in the developing mouse limb

2007 ◽  
Vol 49 (6) ◽  
pp. 515-521 ◽  
Author(s):  
Hsian‐Jean Chin ◽  
Melanie C. Fisher ◽  
Yingcui Li ◽  
Deborah Ferrari ◽  
Chi‐Kuang Leo Wang ◽  
...  
Keyword(s):  
Endochondral Ossification ◽  
Chondrocyte Differentiation ◽  
Mouse Limb

scholarly journals Role of CDMP-1 in Skeletal Morphogenesis: Promotion of Mesenchymal Cell Recruitment and Chondrocyte Differentiation

1999 ◽  
Vol 144 (1) ◽  
pp. 161-173 ◽  
Author(s):  
Noriyuki Tsumaki ◽  
Kazuhiro Tanaka ◽  
Eri Arikawa-Hirasawa ◽  
Takanobu Nakase ◽  
Tomoatsu Kimura ◽  
...  
Keyword(s):  
Endochondral Ossification ◽  
Mesenchymal Cell ◽  
Chondrocyte Differentiation ◽  
Cell Recruitment ◽  
Body Formation ◽  
Morphogenetic Protein ◽  
Chondroprogenitor Cells ◽  
Skeletal Formation ◽  
Targeted Expression

Cartilage provides the template for endochondral ossification and is crucial for determining the length and width of the skeleton. Transgenic mice with targeted expression of recombinant cartilage-derived morphogenetic protein-1 (CDMP-1), a member of the bone morphogenetic protein family, were created to investigate the role of CDMP-1 in skeletal formation. The mice exhibited chondrodysplasia with expanded cartilage, which consists of the enlarged hypertrophic zone and the reduced proliferating chondrocyte zone. Histologically, CDMP-1 increased the number of chondroprogenitor cells and accelerated chondrocyte differentiation to hypertrophy. Expression of CDMP-1 in the notochord inhibited vertebral body formation by blocking migration of sclerotome cells to the notochord. These results indicate that CDMP-1 antagonizes the ventralization signals from the notochord. Our study suggests a molecular mechanism by which CDMP-1 regulates the formation, growth, and differentiation of the skeletal elements.

Effect of ascorbic acid and 1,25(OH)2D3 on bone cell metabolism in relation to the development of tibial dyschondroplasia.

1993 ◽  
Vol 1993 ◽  
pp. 230-230
Author(s):  
C. Farquharso ◽  
J.S. Rennie ◽  
N. Loveridge ◽  
C.C. Whitehead
Keyword(s):  
Ascorbic Acid ◽  
Endochondral Ossification ◽  
Cell Metabolism ◽  
Bone Cell ◽  
Chondrocyte Differentiation ◽  
Fast Growing ◽  
Tibial Dyschondroplasia ◽  
Welfare Implications ◽  
Endogenous Synthesis

Tibial dyschondroplasia (TD) results from a defect in endochondral ossification and is characterised by an accumulation of avascular cartilage extending distally from the growth plate. The lesion develops in young fast growing birds (broilers and turkeys) and is thought to be a result of incomplete chondrocyte differentiation. This condition can result in deformed bones and lameness and has therefore many economic and welfare implications.Since its description 25 years ago, TD has been studied extensively. The majority of the research has focused on determining the role of nutrition in the aetiology of the disease but it has only recently been shown that this disorder can be completely prevented by supplementing the diet with 1,25(OH)2 D3 (Rennie et al., 1993).This may be related to the hormones ability to increase the rate of chondrocyte differentiation (Farquharson et al., 1993). Since ascorbic acid (AA) has been shown previously to stimulate the endogenous synthesis of 1,25(OH)2 D3 (Weiser et al. 1988), its effect on the development of TD in young fast growing broilers was investigated

scholarly journals Osteoclasts promote the formation of hematopoietic stem cell niches in the bone marrow

2012 ◽  
Vol 209 (3) ◽  
pp. 537-549 ◽  
Author(s):  
Anna Mansour ◽  
Grazia Abou-Ezzi ◽  
Ewa Sitnicka ◽  
Sten Eirik W. Jacobsen ◽  
Abdelilah Wakkach ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Hematopoietic Stem Cell ◽  
Endochondral Ossification ◽  
Osteoblastic Differentiation ◽  
Hematopoietic Stem ◽  
Mesenchymal Progenitors ◽  
Hsc Niche ◽  
Niche Formation

Formation of the hematopoietic stem cell (HSC) niche in bone marrow (BM) is tightly associated with endochondral ossification, but little is known about the mechanisms involved. We used the oc/oc mouse, a mouse model with impaired endochondral ossification caused by a loss of osteoclast (OCL) activity, to investigate the role of osteoblasts (OBLs) and OCLs in the HSC niche formation. The absence of OCL activity resulted in a defective HSC niche associated with an increased proportion of mesenchymal progenitors but reduced osteoblastic differentiation, leading to impaired HSC homing to the BM. Restoration of OCL activity reversed the defect in HSC niche formation. Our data demonstrate that OBLs are required for establishing HSC niches and that osteoblastic development is induced by OCLs. These findings broaden our knowledge of the HSC niche formation, which is critical for understanding normal and pathological hematopoiesis.

BMP and Ihh/PTHrP signaling interact to coordinate chondrocyte proliferation and differentiation

Development ◽  
2001 ◽  
Vol 128 (22) ◽  
pp. 4523-4534 ◽  
Author(s):  
Eleonora Minina ◽  
Hans Markus Wenzel ◽  
Conny Kreschel ◽  
Seth Karp ◽  
William Gaffield ◽  
...  
Keyword(s):  
Bone Morphogenetic Proteins ◽  
Feedback Loop ◽  
Bmp Signaling ◽  
Signaling Systems ◽  
Chondrocyte Maturation ◽  
Parathyroid Hormone Related Protein ◽  
Proliferation And Differentiation ◽  
Mouse Limb ◽  
Pthrp Expression

During endochondral ossification, two secreted signals, Indian hedgehog (Ihh) and parathyroid hormone-related protein (PTHrP), have been shown to form a negative feedback loop regulating the onset of hypertrophic differentiation of chondrocytes. Bone morphogenetic proteins (BMPs), another family of secreted factors regulating bone formation, have been implicated as potential interactors of the Ihh/PTHrP feedback loop. To analyze the relationship between the two signaling pathways, we used an organ culture system for limb explants of mouse and chick embryos. We manipulated chondrocyte differentiation by supplementing these cultures either with BMP2, PTHrP and Sonic hedgehog as activators or with Noggin and cyclopamine as inhibitors of the BMP and Ihh/PTHrP signaling systems. Overexpression of Ihh in the cartilage elements of transgenic mice results in an upregulation of PTHrP expression and a delayed onset of hypertrophic differentiation. Noggin treatment of limbs from these mice did not antagonize the effects of Ihh overexpression. Conversely, the promotion of chondrocyte maturation induced by cyclopamine, which blocks Ihh signaling, could not be rescued with BMP2. Thus BMP signaling does not act as a secondary signal of Ihh to induce PTHrP expression or to delay the onset of hypertrophic differentiation. Similar results were obtained using cultures of chick limbs. We further investigated the role of BMP signaling in regulating proliferation and hypertrophic differentiation of chondrocytes and identified three functions of BMP signaling in this process. First we found that maintaining a normal proliferation rate requires BMP and Ihh signaling acting in parallel. We further identified a role for BMP signaling in modulating the expression of Ihh. Finally, the application of Noggin to mouse limb explants resulted in advanced differentiation of terminally hypertrophic cells, implicating BMP signaling in delaying the process of hypertrophic differentiation itself. This role of BMP signaling is independent of the Ihh/PTHrP pathway.

scholarly journals Non-Coding RNAs in Cartilage Development: An Updated Review

2019 ◽  
Vol 20 (18) ◽  
pp. 4475 ◽  
Author(s):  
Ehsan Razmara ◽  
Amirreza Bitaraf ◽  
Hassan Yousefi ◽  
Tina H. Nguyen ◽  
Masoud Garshasbi ◽  
...  
Keyword(s):  
Cell Biology ◽  
Endochondral Ossification ◽  
Association Studies ◽  
Post Translational Modifications ◽  
Cartilage Development ◽  
Complex Process ◽  
Cartilage Cells ◽  
Non Coding Rnas ◽  
Skeletal Disorders

In the development of the skeleton, the long bones are arising from the process of endochondral ossification (EO) in which cartilage is replaced by bone. This complex process is regulated by various factors including genetic, epigenetic, and environmental elements. It is recognized that DNA methylation, higher-order chromatin structure, and post-translational modifications of histones regulate the EO. With emerging understanding, non-coding RNAs (ncRNAs) have been identified as another mode of EO regulation, which is consist of microRNAs (miRNAs or miRs) and long non-coding RNAs (lncRNAs). There is expanding experimental evidence to unlock the role of ncRNAs in the differentiation of cartilage cells, as well as the pathogenesis of several skeletal disorders including osteoarthritis. Cutting-edge technologies such as epigenome-wide association studies have been employed to reveal disease-specific patterns regarding ncRNAs. This opens a new avenue of our understanding of skeletal cell biology, and may also identify potential epigenetic-based biomarkers. In this review, we provide an updated overview of recent advances in the role of ncRNAs especially focus on miRNA and lncRNA in the development of bone from cartilage, as well as their roles in skeletal pathophysiology.

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 G-proteins in the differentiation of epiphyseal chondrocytes

2014 ◽  
Vol 53 (2) ◽  
pp. R39-R45 ◽  
Author(s):  
Andrei S Chagin ◽  
Henry M Kronenberg
Keyword(s):  
G Protein ◽  
G Proteins ◽  
Growth Plate ◽  
Current Knowledge ◽  
Postnatal Growth ◽  
Chondrocyte Differentiation ◽  
Growth Plate Chondrocytes ◽  
Α Subunit ◽  
G Protein Coupled

Herein, we review the regulation of differentiation of the growth plate chondrocytes by G-proteins. In connection with this, we summarize the current knowledge regarding each family of G-protein α subunit, specifically, Gαs, Gαq/11, Gα12/13, and Gαi/o. We discuss different mechanisms involved in chondrocyte differentiation downstream of G-proteins and different G-protein-coupled receptors (GPCRs) activating G-proteins in the epiphyseal chondrocytes. We conclude that among all G-proteins and GPCRs expressed by chondrocytes, Gαshas the most important role and prevents premature chondrocyte differentiation. Receptor for parathyroid hormone (PTHR1) appears to be the major activator of Gαsin chondrocytes and ablation of either one leads to accelerated chondrocyte differentiation, premature fusion of the postnatal growth plate, and ultimately short stature.

scholarly journals Role of 5′HOXD genes in the endochondral ossification

2011 ◽  
Vol 356 (1) ◽  
pp. 235
Author(s):  
Carmen González-Martín ◽  
Carlos Garrido-Allepuz ◽  
Marian Ros
Keyword(s):  
Endochondral Ossification
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