scholarly journals On the role of type IX collagen in the extracellular matrix of cartilage: type IX collagen is localized to intersections of collagen fibrils.

1986 ◽  
Vol 102 (5) ◽  
pp. 1931-1939 ◽  
Author(s):  
W Müller-Glauser ◽  
B Humbel ◽  
M Glatt ◽  
P Sträuli ◽  
K H Winterhalter ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Bone Formation ◽  
Tissue Distribution ◽  
Chicken Embryo ◽  
Polyclonal Antibodies ◽  
Type Ii Collagen ◽  
Endochondral Bone Formation ◽  
Type Ii ◽  
Endochondral Bone

The tissue distribution of type II and type IX collagen in 17-d-old chicken embryo was studied by immunofluorescence using polyclonal antibodies against type II collagen and a peptic fragment of type IX collagen (HMW), respectively. Both proteins were found only in cartilage where they were co-distributed. They occurred uniformly throughout the extracellular matrix, i.e., without distinction between pericellular, territorial, and interterritorial matrices. Tissues that undergo endochondral bone formation contained type IX collagen, whereas periosteal and membranous bones were negative. The thin collagenous fibrils in cartilage consisted of type II collagen as determined by immunoelectron microscopy. Type IX collagen was associated with the fibrils but essentially was restricted to intersections of the fibrils. These observations suggested that type IX collagen contributes to the stabilization of the network of thin fibers of the extracellular matrix of cartilage by interactions of its triple helical domains with several fibrils at or close to their intersections.

scholarly journals Parathyroid hormone-related peptide-depleted mice show abnormal epiphyseal cartilage development and altered endochondral bone formation.

1994 ◽  
Vol 126 (6) ◽  
pp. 1611-1623 ◽  
Author(s):  
N Amizuka ◽  
H Warshawsky ◽  
J E Henderson ◽  
D Goltzman ◽  
A C Karaplis
Keyword(s):  
Bone Formation ◽  
Embryonic Stem ◽  
Type Ii Collagen ◽  
Epiphyseal Plate ◽  
Epiphyseal Cartilage ◽  
Endochondral Bone Formation ◽  
Type Ii ◽  
Endochondral Bone ◽  
Cartilage Development ◽  
Calcified Cartilage

To elucidate the role of PTHrP in skeletal development, we examined the proximal tibial epiphysis and metaphysis of wild-type (PTHrP-normal) 18-19-d-old fetal mice and of chondrodystrophic litter mates homozygous for a disrupted PTHrP allele generated via homologous recombination in embryonic stem cells (PTHrP-depleted). In the PTHrP-normal epiphysis, immunocytochemistry showed PTHrP to be localized in chondrocytes within the resting zone and at the junction between proliferative and hypertrophic zones. In PTHrP-depleted epiphyses, a diminished [3H]thymidine-labeling index was observed in the resting and proliferative zones accounting for reduced numbers of epiphyseal chondrocytes and for a thinner epiphyseal plate. In the mutant hypertrophic zone, enlarged chondrocytes were interspersed with clusters of cells that did not hypertrophy, but resembled resting or proliferative chondrocytes. Although the overall content of type II collagen in the epiphyseal plate was diminished, the lacunae of these non-hypertrophic chondrocytes did react for type II collagen. Moreover, cell membrane-associated chondroitin sulfate immunoreactivity was evident on these cells. Despite the presence of alkaline phosphatase activity on these nonhypertrophic chondrocytes, the adjacent cartilage matrix did not calcify and their persistence accounted for distorted chondrocyte columns and sporadic distribution of calcified cartilage. Consequently, in the metaphysis, bone deposited on the irregular and sparse scaffold of calcified cartilage and resulted in mixed spicules that did not parallel the longitudinal axis of the tibia and were, therefore, inappropriate for bone elongation. Thus, PTHrP appears to modulate both the proliferation and differentiation of chondrocytes and its absence alters the temporal and spatial sequence of epiphyseal cartilage development and of subsequent endochondral bone formation necessary for normal elongation of long bones.

CARTILAGE-SPECIFIC OVEREXPRESSION OF C-PROPEPTIDE OF TYPE II COLLAGEN AFFECTED MATRIX MINERALIZATION IN TRANSGENIC MICE

2003 ◽  
Vol 07 (03n04) ◽  
pp. 183-189
Author(s):  
Yoshito Matsui ◽  
Ken Nakata ◽  
Eijiro Adachi ◽  
Noriyuki Tsumaki ◽  
Tomoatsu Kimura ◽  
...  
Keyword(s):  
Bone Formation ◽  
Transgenic Mice ◽  
Growth Plate ◽  
Type Ii Collagen ◽  
Whole Body ◽  
Endochondral Bone Formation ◽  
Type Ii ◽  
Endochondral Bone ◽  
Matrix Mineralization ◽  
Growth Plate Cartilage

The C-propeptide of type II collagen (CppII) is cleaved from the procollagen molecule at the time of extracellular secretion from chondrocytes, and was reported to localize in the lower hypertrophic zone of the growth plate cartilage. In the present study, the in vivo role of CppII in the process of endochondral bone formation was investigated by cartilage-specific overexpression of CppII in transgenic mice. Two independent lines of transgenic mice were obtained and they showed mild skeletal dysplasia, as evidenced by morphometric measurement of skeletal bones. Whole body staining revealed delayed mineralization of embryonic endochondral bones, including occipital bone and vertebral bodies. Histological sections showed reduced area of mineralization and scattered chondrocyte hypertrophy in the lower part of growth plate cartilage in the embryonic long bones. Immuno-electron micrographs demonstrated that CppII co-localized with collagen fibrils in the extracellular matrix of the cartilage. Taken together, these results indicate that overexpression of CppII affected endochondral bone formation by negatively regulating the matrix mineralization.

The role of Akt1 in terminal stages of endochondral bone formation: Angiogenesis and ossification

Bone ◽  
2009 ◽  
Vol 45 (6) ◽  
pp. 1133-1145 ◽  
Author(s):  
Veronica Ulici ◽  
Katie D. Hoenselaar ◽  
Hanga Agoston ◽  
David D. McErlain ◽  
Joseph Umoh ◽  
...  
Keyword(s):  
Bone Formation ◽  
Endochondral Bone Formation ◽  
Endochondral Bone

ENDOCHONDRAL BONE FORMATION AND EXTRACELLULAR MATRIX

2005 ◽  
pp. 145-162
Author(s):  
Qian Chen ◽  
Lei Wei ◽  
Zhengke Wang ◽  
Xiaojuan Sun ◽  
Junming Luo ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Bone Formation ◽  
Endochondral Bone Formation ◽  
Endochondral Bone

scholarly journals Expression and Role of IL-1β Signaling in Chondrocytes Associated with Retinoid Signaling during Fracture Healing

2020 ◽  
Vol 21 (7) ◽  
pp. 2365 ◽  
Author(s):  
Tsuyoshi Shimo ◽  
Hiroaki Takebe ◽  
Tatsuo Okui ◽  
Yuki Kunisada ◽  
Soichiro Ibaragi ◽  
...  
Keyword(s):  
Bone Formation ◽  
Fracture Healing ◽  
P38 Mapk ◽  
Inverse Agonist ◽  
Endochondral Bone Formation ◽  
Dependent Manner ◽  
Retinoid Receptor ◽  
Endochondral Bone ◽  
Inverse Agonists

The process of fracture healing consists of an inflammatory reaction and cartilage and bone tissue reconstruction. The inflammatory cytokine interleukin-1β (IL-1β) signal is an important major factor in fracture healing, whereas its relevance to retinoid receptor (an RAR inverse agonist, which promotes endochondral bone formation) remains unclear. Herein, we investigated the expressions of IL-1β and retinoic acid receptor gamma (RARγ) in a rat fracture model and the effects of IL-1β in the presence of one of several RAR inverse agonists on chondrocytes. An immunohistochemical analysis revealed that IL-1β and RARγ were expressed in chondrocytes at the fracture site in the rat ribs on day 7 post-fracture. In chondrogenic ATDC5 cells, IL-1β decreases the levels of aggrecan and type II collagen but significantly increased the metalloproteinase-13 (Mmp13) mRNA by real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis. An RAR inverse agonist (AGN194310) inhibited IL-1β-stimulated Mmp13 and Ccn2 mRNA in a dose-dependent manner. Phosphorylated extracellular signal regulated-kinases (pERK1/2) and p-p38 mitogen-activated protein kinase (MAPK) were increased time-dependently by IL-1β treatment, and the IL-1β-induced p-p38 MAPK was inhibited by AGN194310. Experimental p38 inhibition led to a drop in the IL-1β-stimulated expressions of Mmp13 and Ccn2 mRNA. MMP13, CCN2, and p-p38 MAPK were expressed in hypertrophic chondrocytes near the invaded vascular endothelial cells. As a whole, these results point to role of the IL-1β via p38 MAPK as important signaling in the regulation of the endochondral bone formation in fracture healing, and to the actions of RAR inverse agonists as potentially relevant modulators of this process.

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