Differential regulation of type-II and type-X collagen synthesis by parathyroid hormone-related protein in chick growth-plate chondrocytes

1997 ◽  
Vol 15 (2) ◽  
pp. 162-174 ◽  
Author(s):  
Regis J. O'Keefe ◽  
Luke S. Loveys ◽  
David G. Hicks ◽  
Paul R. Reynolds ◽  
Ian D. Crabb ◽  
...  
1993 ◽  
Vol 11 (6) ◽  
pp. 884-891 ◽  
Author(s):  
Luke S. Loveys ◽  
Daniel Gelb ◽  
Shepard R. Hurwitz ◽  
J. Edward Puzas ◽  
Randy N. Rosier

1991 ◽  
Vol 277 (2) ◽  
pp. 513-520 ◽  
Author(s):  
G J Gibson ◽  
K T Francki ◽  
J J Hopwood ◽  
B K Foster

Direct comparison of type X collagen synthesized by human, sheep and chick growth-plate cartilage has shown that the human type X collagen is similar to the chick in both its molecular mass, containing component alpha-chains of 59 kDa with helical regions of 45 kDa, and apparent absence of disulphide-stabilized aggregates, whereas the sheep type X collagen has slightly larger alpha-chains (63 kDa) accounted for by a longer helical region (49 kDa) that contains cystine residues essential for the formation of the high-molecular-mass aggregates found with this species. Type X collagen from all three species showed heterogeneity in primary collagen structure as revealed by Staphylococcus aureus V8 proteinase-generated peptide maps. Collagen synthesis by growth-plate cartilage in culture, particularly synthesis of type IX and X collagen, was shown to be very sensitive to prior storage and suggests caution in the interpretation of changes detected when examining collagen synthesis by growth plates in culture.


2002 ◽  
Vol 283 (1) ◽  
pp. L12-L21 ◽  
Author(s):  
Randolph H. Hastings ◽  
Angela Asirvatham ◽  
Rick Quintana ◽  
Rebeca Sandoval ◽  
Ruchika Dutta ◽  
...  

Inhalation of silica leads to acute lung injury and alveolar type II cell proliferation. Type II cell proliferation after hyperoxic lung injury is regulated, in part, by parathyroid hormone-related protein (PTHrP). In this study, we investigated lung PTHrP and its effects on epithelial proliferation after injury induced by silica. Lung PTHrP decreased modestly 4 days after we instilled 10 mg of silica into rat lungs and then recovered from 4 to 28 days. The number of proliferating cell nuclear antigen (PCNA)-positive type II cells was increased threefold in silica-injured lungs compared with controls. Subsequently, rats were treated with four exogenous PTHrP peptides in the silica instillate, which were administered subcutaneously daily. One peptide, PTHrP-(38–64), had consistent and significant effects on cell proliferation. PTHrP-(38–64) increased the median number of PCNA-positive cells/field nearly fourfold above controls, 380 vs. 109 ( P < 0.05). Thymidine incorporation was 2.5 times higher in type II cells isolated from rats treated with PTHrP-(38–64) compared with PBS. PTHrP-(38–64) significantly increased the number of cells expressing alkaline phosphatase, a type II cell marker. This study indicates that PTHrP-(38–64) stimulates type II cell growth and may have a role in lung repair in silica-injured rats.


2011 ◽  
Vol 47 (1) ◽  
pp. 99-107 ◽  
Author(s):  
Michael Chau ◽  
Patricia Forcinito ◽  
Anenisia C Andrade ◽  
Anita Hegde ◽  
Sohyun Ahn ◽  
...  

In embryonic growth cartilage, Indian hedgehog (Ihh) and parathyroid hormone-related protein (PTHrP) participate in a negative feedback loop that regulates chondrocyte differentiation. Postnatally, this region undergoes major structural and functional changes. To explore the organization of the Ihh–PTHrP system in postnatal growth plate, we microdissected growth plates of 7-day-old rats into their constituent zones and assessed expression of genes participating in the Ihh–PTHrP feedback loop.Ihh, Patched 1, Smoothened,Gli1, Gli2, Gli3, andPthr1were expressed in regions analogous to the expression domains in embryonic growth cartilage. However, PTHrP was expressed in resting zone cartilage, a site that differs from the embryonic source, the periarticular cells. We then used mice in whichlacZhas replaced coding sequences ofGli1and thus serves as a marker for active hedgehog signaling. At 1, 4, 8, and 12 weeks of age,lacZexpression was detected in a pattern analogous to that of embryonic cartilage. The findings support the hypothesis that the embryonic Ihh–PTHrP feedback loop is maintained in the postnatal growth plate except that the source of PTHrP has shifted to a more proximal location in the resting zone.


2002 ◽  
Vol 282 (6) ◽  
pp. L1198-L1208 ◽  
Author(s):  
Randolph H. Hastings ◽  
Rita M. Ryan ◽  
Carl T. D'Angio ◽  
Bruce A. Holm ◽  
Alka Patel ◽  
...  

Parathyroid hormone-related protein (PTHrP) is a growth inhibitor for alveolar type II cells. Type II cell proliferation after lung injury from 85% oxygen is regulated, in part, by a fall in lung PTHrP. In this study, we investigated lung PTHrP after injury induced by >95% oxygen in rats and rabbits. In adult rats, lung PTHrP rose 10-fold over controls to 6,356 ± 710 pg/ml (mean ± SE) at 48 h of hyperoxia. Levels fell to 299 ± 78 pg/ml, and staining for PTHrP mRNA was greatly reduced at 60 h ( P < 0.05), the point of most severe injury and greatest pneumocyte proliferation. In adult rabbits, lung PTHrP peaked at 3,289 ± 230 pg/ml after 64 h of hyperoxia with 24 h of normoxic recovery and then dropped to 1,629 ± 153 pg/ml at 48 h of recovery ( P < 0.05). Type II cell proliferation peaked shortly after the fall in PTHrP. In newborn rabbits, lavage PTHrP increased by 50% during the first 8 days of hyperoxia, whereas type II cell growth decreased. PTHrP declined at the LD50, concurrent with increased type II cell division. In summary, lung PTHrP initially rises after injury with >95% hyperoxia and then falls near the peak of injury. Changes in PTHrP are temporally related to type II cell proliferation and may regulate repair of lung injury.


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