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Culturing and Measuring Fetal and Newborn Murine Long Bones
Published on: April 26, 2019
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ADAM10 is indispensable for longitudinal bone growth in mice
Sakiko Mizuno1, Masaki Yoda2, Tokuhiro Kimura3
1Department of Orthopedic Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan; Department of Orthopedics, Tokyo Dental College Ichikawa General Hospital, 5-11-13 Sugano, Ichikawa City, Chiba 272-8513, Japan.
Bone
|February 17, 2020
Summary
ADAM10, a protease, is crucial for skeletal development and long bone growth. Its absence impairs chondrocyte function and growth, highlighting a new role in regulating the CXCL12/CXCR4 pathway.
Area of Science:
- Molecular Biology
- Developmental Biology
- Biochemistry
Background:
- Skeletal development relies on precise regulation of growth factors and signaling molecules.
- ADAM10 (a disintegrin and metalloproteinase domain 10) is a protease involved in regulating membrane-bound proteins.
Purpose of the Study:
- To investigate the role of ADAM10 in skeletal development and longitudinal bone growth.
- To elucidate the molecular mechanisms underlying ADAM10's function in the growth plate.
Main Methods:
- Generation and analysis of mice lacking ADAM10 in osteochondroprogenitors.
- Histomorphometric analysis of long bones and growth plates.
- Gene expression analysis (mRNA) of chemokines and their receptors.
- Ex vivo culture of growth plate explants with CXCL12 supplementation.
Main Results:
- Mice lacking ADAM10 in osteochondroprogenitors showed growth retardation and shorter long bones.
- Histomorphometry revealed a reduced hypertrophic zone and smaller hypertrophic chondrocytes in mutants.
- ADAM10 deficiency led to decreased mRNA expression of CXCL12 and CXCR4 in cartilage.
- Recombinant CXCL12 rescued growth plate defects in an ex vivo model.
Conclusions:
- ADAM10 plays a critical, previously unrecognized role in longitudinal bone growth and skeletal development.
- ADAM10 regulates skeletal development through the CXCL12/CXCR4 signaling pathway.
- Targeting ADAM10 or the CXCL12/CXCR4 pathway may offer therapeutic strategies for skeletal disorders.
