PTH Receptor Signaling in Osteoblasts Regulates Endochondral Vascularization in Maintenance of Postnatal Growth Plate
Year: 2014
Type: article
Abstract: Longitudinal growth of postnatal bone requires precise control of growth plate cartilage chondrocytes and subsequent osteogenesis and bone formation. Little is known about the role of angiogenesis and bone remodeling in maintenance of cartilaginous growth plate. Parathyroid hormone (PTH) stimulates bone remodeling by activating PTH receptor (PTH1R). Mice with conditional deletion of PTH1R in osteoblasts showed disrupted trabecular bone formation. The mice also exhibited postnatal growth retardation with profound defects in growth plate cartilage, ascribable predominantly to a decrease in number of hypertrophic chondrocytes, resulting in premature fusion of the growth plate and shortened long bones. Further characterization of hypertrophic zone and primary spongiosa revealed that endochondral angiogenesis and vascular invasion of the cartilage were impaired, which was associated with aberrant chondrocyte maturation and cartilage development. These studies reveal that PTH1R signaling in osteoblasts regulates cartilaginous growth plate for postnatal growth of bone.
DOI: 10.1002/jbmr.2327
Language: English
Topic: Bone Metabolism and Diseases
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
Awards: Notch Signaling in Joint Cartilage Maintenance and Arthritis, TGF-beta Activity in the Subchondral Bone and Onset of OA, G4912936831, G5030237289, Phosphorylation of PTH1R by TGF-betaRII in Bone Remodeling, G6538829004, Function Of DNA Virus Genomes In Animal Cells, G858913493, Mechanism of Smad1 Mediated Osteoblast Differentiation, Notch Signaling in Cartilage Development, G9000079241
OpenAlex ID: W1549662004