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The extracellular calcium-sensing receptor (CaSR) is a critical modulator of skeletal development

Wenhan Chang1, Chialing Tu, Tsui-Hua Chen

  • 1Endocrine Research Unit, Department of Veterans Affairs Medical Center, Department of Medicine, University of California, San Francisco, CA 94121, USA. wenhan.chang@ucsf.edu

Science Signaling
|September 4, 2008
PubMed

Insights

The calcium-sensing receptor (CaSR) is crucial for parathyroid gland and kidney function. Its deletion in mice causes severe skeletal defects and impacts early development, highlighting its critical role in embryogenesis and bone formation.

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Skeletal Biology

Background:

  • The extracellular calcium-sensing receptor (CaSR) is vital for parathyroid gland (PTG) and kidney function.
  • Previous studies using global Casr knockout mice were limited by severe phenotypes, preventing tissue-specific analysis.

Purpose of the Study:

  • To investigate the tissue-specific roles of CaSR in PTG, bone, and cartilage during development.
  • To elucidate the CaSR's function in early embryogenesis and skeletal development.

Main Methods:

  • Generation of mice with tissue-specific deletion of the Casr gene in the PTG, bone, and chondrocytes.
  • Analysis of developmental phenotypes, including embryonic lethality, skeletal defects, and growth plate development.

Main Results:

  • Deletion of Casr in the PTG or bone led to significant bone defects.
  • Chondrocyte-specific Casr deletion caused embryonic lethality before E13.
  • Delayed growth plate development was observed in mice with late-induced chondrocyte-specific Casr deletion.

Conclusions:

  • The CaSR plays a critical, nonredundant role in early embryogenesis.
  • CaSR is essential for normal skeletal development, particularly in chondrocytes and bone.
  • Tissue-specific roles of CaSR are vital for understanding its broader physiological functions.

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