Calcium-Sensing Receptor Deficiency Affects Bone and Cartilage Development in Mice
Author Information
Author(s): Liu Jingning, Lv Fangqiao, Sun Wen, Tao Chunxiang, Ding Guoxian, Karaplis Andrew, Brown Edward, Goltzman David, Miao Dengshun
Primary Institution: Nanjing Medical University
Hypothesis
What are the effects of calcium-sensing receptor deficiency on skeletal development and calcium homeostasis?
Conclusion
Calcium-sensing receptor deficiency in mice leads to severe skeletal growth retardation and abnormalities, which can be partially rescued by the deletion of parathyroid hormone.
Supporting Evidence
- CaR-deficient mice displayed hypercalcemia, hypophosphatemia, and severe skeletal growth retardation.
- Deletion of PTH in CaR-deficient mice resulted in normalization of skeletal growth.
- Ablation of 1α(OH)ase in CaR-deficient mice improved lifespan and body weight.
- Chondrocyte proliferation was significantly reduced in CaR-deficient mice.
Takeaway
Mice without the calcium-sensing receptor have serious problems with their bones and growth, but removing parathyroid hormone helps them grow better.
Methodology
The study compared skeletal phenotypes of CaR-deficient mice with those of double homozygous CaR- and 1α(OH)ase-deficient or CaR- and PTH-deficient mice at 2 weeks of age.
Limitations
The study primarily focuses on a mouse model, which may not fully replicate human conditions.
Participant Demographics
Mice were used in the study, specifically homozygous CaR-deficient mice and various knockout models.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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