scholarly journals Targeted overexpression of parathyroid hormone-related peptide in chondrocytes causes chondrodysplasia and delayed endochondral bone formation.

1996 ◽  
Vol 93 (19) ◽  
pp. 10240-10245 ◽  
Author(s):  
E. C. Weir ◽  
W. M. Philbrick ◽  
M. Amling ◽  
L. A. Neff ◽  
R. Baron ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Formation ◽  
Endochondral Bone Formation ◽  
Endochondral Bone ◽  
Related Peptide ◽  
Parathyroid Hormone Related Peptide

scholarly journals Parathyroid hormone-related peptide delays terminal differentiation of chondrocytes during endochondral bone development.

Endocrinology ◽  
1996 ◽  
Vol 137 (11) ◽  
pp. 5109-5118 ◽  
Author(s):  
K Lee ◽  
B Lanske ◽  
A C Karaplis ◽  
J D Deeds ◽  
H Kohno ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Development ◽  
Terminal Differentiation ◽  
Endochondral Bone ◽  
Related Peptide ◽  
Parathyroid Hormone Related Peptide

scholarly journals The C-terminal fragment of parathyroid hormone-related peptide promotes bone formation in diabetic mice with low-turnover osteopaenia

2011 ◽  
Vol 162 (6) ◽  
pp. 1424-1438 ◽  
Author(s):  
D Lozano ◽  
L Fernández-de-Castro ◽  
S Portal-Núñez ◽  
A López-Herradón ◽  
S Dapía ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Formation ◽  
Diabetic Mice ◽  
Related Peptide ◽  
Terminal Fragment ◽  
Parathyroid Hormone Related Peptide

scholarly journals Parathyroid Hormone–related Peptide (PTHrP)-dependent and -independent Effects of Transforming Growth Factor β (TGF-β) on Endochondral Bone Formation

1999 ◽  
Vol 145 (4) ◽  
pp. 783-794 ◽  
Author(s):  
Rosa Serra ◽  
Andrew Karaplis ◽  
Philip Sohn
Keyword(s):  
Bone Formation ◽  
Transforming Growth Factor ◽  
Terminal Differentiation ◽  
Transforming Growth Factor Β ◽  
Endochondral Bone Formation ◽  
Endochondral Bone ◽  
Matrix Mineralization ◽  
Parathyroid Hormone Related Peptide ◽  
Independent Effects

Previously, we showed that expression of a dominant-negative form of the transforming growth factor β (TGF-β) type II receptor in skeletal tissue resulted in increased hypertrophic differentiation in growth plate and articular chondrocytes, suggesting a role for TGF-β in limiting terminal differentiation in vivo. Parathyroid hormone–related peptide (PTHrP) has also been demonstrated to regulate chondrocyte differentiation in vivo. Mice with targeted deletion of the PTHrP gene demonstrate increased endochondral bone formation, and misexpression of PTHrP in cartilage results in delayed bone formation due to slowed conversion of proliferative chondrocytes into hypertrophic chondrocytes. Since the development of skeletal elements requires the coordination of signals from several sources, this report tests the hypothesis that TGF-β and PTHrP act in a common signal cascade to regulate endochondral bone formation. Mouse embryonic metatarsal bone rudiments grown in organ culture were used to demonstrate that TGF-β inhibits several stages of endochondral bone formation, including chondrocyte proliferation, hypertrophic differentiation, and matrix mineralization. Treatment with TGF-β1 also stimulated the expression of PTHrP mRNA. PTHrP added to cultures inhibited hypertrophic differentiation and matrix mineralization but did not affect cell proliferation. Furthermore, terminal differentiation was not inhibited by TGF-β in metatarsal rudiments from PTHrP-null embryos; however, growth and matrix mineralization were still inhibited. The data support the model that TGF-β acts upstream of PTHrP to regulate the rate of hypertrophic differentiation and suggest that TGF-β has both PTHrP-dependent and PTHrP-independent effects on endochondral bone formation.

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