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Updated: Jul 9, 2026

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
Published on: April 1, 2022
Development of craniofacial structures in transgenic mice with constitutively active PTH/PTHrP receptor
T W Tsutsui1, M Riminucci, Kenn Holmbeck
1Craniofacial and Skeletal Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Department Health Human Services, Bethesda, MD 20892, USA. ryuryu@tokyo.ndu.ac.jp
A new transgenic mouse model with a constitutively active parathyroid hormone (PTH) receptor shows significant craniofacial and dental abnormalities during development. This model aids in studying receptor effects on hard tissue formation and related human diseases.
Area of Science:
- Endocrinology and Developmental Biology
- Skeletal Biology
- Craniofacial Development
Background:
- Parathyroid hormone (PTH) and parathyroid hormone-related peptide (PTHrP) are key regulators of calcium homeostasis.
- PTHrP also plays a crucial role in growth, development, and hard tissue formation.
- Dysregulation of PTH/PTHrP signaling can lead to skeletal abnormalities.
Purpose of the Study:
- To characterize craniofacial developmental abnormalities in a novel transgenic mouse model (Col1-caPPR) expressing a constitutively active PTH/PTHrP receptor.
- To investigate the role of the active PTH/PTHrP receptor in hard tissue formation and development.
- To establish a valuable model for studying diseases with similar craniofacial and skeletal phenotypes.
Main Methods:
- Development of a transgenic mouse (Col1-caPPR) with a constitutively active PTH/PTHrP receptor driven by the alpha1(I) collagen promoter.
- Detailed characterization of craniofacial abnormalities throughout the developmental stages of these mice.
- Analysis of bone formation, tooth eruption, and temporomandibular joint (TMJ) development.
Main Results:
- Col1-caPPR mice displayed delayed embryonic bone formation.
- Significant expansion of craniofacial bones, including the maxilla and mandible, was observed.
- Delayed tooth eruption, teratosis, and temporomandibular joint (TMJ) disruption were prominent features.
Conclusions:
- The Col1-caPPR mouse model effectively demonstrates the complex actions of a constitutively active PTH/PTHrP receptor in hard tissue formation.
- This model provides insights into developmental and growth processes regulated by PTH/PTHrP signaling.
- The Col1-caPPR mouse serves as a valuable tool for understanding and potentially treating human diseases with related characteristics.

