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  • 1
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    Regulation of rate of cartilage differentiation by Indian hedgehog and PTH-related protein (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: Proper regulation of chondrocyte differentiation is necessary for the morphogenesis of skeletal elements, yet little is known about the molecular regulation of this process. A chicken homolog of Indian hedgehog (Ihh), a member of the conserved Hedgehog family of secreted proteins that is expressed during bone formation, has now been isolated. Ihh has biological properties similar to those of Sonic hedgehog (Shh), including the ability to regulate the conserved targets Patched (Ptc) and Gli. Ihh is expressed in the prehypertrophic chondrocytes of cartilage elements, where it regulates the rate of hypertrophic differentiation. Misexpression of Ihh prevents proliferating chondrocytes from initiating the hypertrophic differentiation process. The direct target of Ihh signaling is the perichondrium, where Gli and Ptc flank the expression domain of Ihh. Ihh induces the expression of a second signal, parathyroid hormone-related protein (PTHrP), in the periarticular perichondrium. Analysis of PTHrP (-/-) mutant mice indicated that the PTHrP protein signals to its receptor in the prehypertrophic chondrocytes, thereby blocking hypertrophic differentiation. In vitro application of Hedgehog or PTHrP protein to normal or PTHrP (-/-) limb explants demonstrated that PTHrP mediates the effects of Ihh through the formation of a negative feedback loop that modulates the rate of chondrocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vortkamp, A -- Lee, K -- Lanske, B -- Segre, G V -- Kronenberg, H M -- Tabin, C J -- DK47038/DK/NIDDK NIH HHS/ -- DK4723/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):613-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Bone Development ; Cartilage/*cytology/metabolism ; Cell Differentiation ; Cell Division ; Chick Embryo ; Cloning, Molecular ; Culture Techniques ; Extremities/embryology ; Feedback ; Gene Expression Regulation ; Growth Plate/*cytology/metabolism ; Hedgehog Proteins ; Mice ; Molecular Sequence Data ; Morphogenesis ; *Osteogenesis ; Parathyroid Hormone ; Parathyroid Hormone-Related Protein ; Phenotype ; Proteins/pharmacology/*physiology ; Receptor, Parathyroid Hormone, Type 1 ; Receptors, Parathyroid Hormone/physiology ; Signal Transduction ; *Trans-Activators
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    PTH/PTHrP receptor in early development and Indian hedgehog-regulated bone growth (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-08-02
    Description: The PTH/PTHrP receptor binds to two ligands with distinct functions: the calcium-regulating hormone, parathyroid hormone (PTH), and the paracrine factor, PTH-related protein (PTHrP). Each ligand, in turn, is likely to activate more than one receptor. The functions of the PTH/PTHrP receptor were investigated by deletion of the murine gene by homologous recombination. Most PTH/PTHrP receptor (-/-) mutant mice died in mid-gestation, a phenotype not observed in PTHrP (-/-) mice, perhaps because of the effects of maternal PTHrP. Mice that survived exhibited accelerated differentiation of chondrocytes in bone, and their bones, grown in explant culture, were resistant to the effects of PTHrP and Sonic hedgehog. These results suggest that the PTH/PTHrP receptor mediates the effects of Indian Hedgehog and PTHrP on chondrocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lanske, B -- Karaplis, A C -- Lee, K -- Luz, A -- Vortkamp, A -- Pirro, A -- Karperien, M -- Defize, L H -- Ho, C -- Mulligan, R C -- Abou-Samra, A B -- Juppner, H -- Segre, G V -- Kronenberg, H M -- DK 47038/DK/NIDDK NIH HHS/ -- DK 47237/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Aug 2;273(5275):663-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8662561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Development ; Cartilage/*cytology/metabolism ; Cell Differentiation ; Cell Division ; Cloning, Molecular ; Culture Techniques ; Feedback ; Gene Deletion ; Gene Targeting ; Growth Plate/*cytology/metabolism ; Hedgehog Proteins ; Mice ; Mice, Inbred C57BL ; Osteoblasts/cytology ; *Osteogenesis ; Parathyroid Hormone ; Parathyroid Hormone-Related Protein ; Protein Biosynthesis ; Proteins/pharmacology/physiology ; Receptor, Parathyroid Hormone, Type 1 ; Receptors, Parathyroid Hormone/genetics/*physiology ; Stem Cells ; *Trans-Activators
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
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