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PDGF mediates TGFβ-induced migration during development of the spinous process
1Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL, USA.
Developmental Biology
|February 29, 2012
Summary
Transforming growth factor beta (TGFβ) signaling regulates vertebral development. Loss of TGFβ type II receptor (Tgfbr2) in mice causes spinal defects by impairing mesenchymal cell migration, mediated by platelet-derived growth factor (PDGF).
Area of Science:
- Developmental Biology
- Molecular Biology
- Skeletal Biology
Background:
- Mechanisms of dorsal vertebrae closure are not fully understood.
- Deletion of TGFβ type II receptor (Tgfbr2) in mouse sclerotome leads to spinous process formation failure, resembling human spina bifida occulta.
Purpose of the Study:
- To investigate if dorsal structure defects in Tgfbr2 mutant mice result from impaired mesenchymal migration.
- To elucidate the mechanism of TGFβ-mediated cell migration in vertebral development.
Main Methods:
- Analysis of dorsal vertebrae development in Tgfbr2 mutant mice at E16.5.
- Histological examination of sclerotome and adjacent mesenchyme.
- Chemotaxis migration assays using mixed cultures of embryonic sclerotome and mesenchyme.
- Assessment of PDGF ligand and receptor expression and signaling.
Main Results:
- Tgfbr2 mutant mice exhibited gross alterations in dorsal vertebrae by E16.5.
- Histology revealed thinner mesenchyme adjacent to cartilage in mutants, indicating reduced cell proliferation and migration.
- TGFβ promoted migration in vitro and stimulated PDGF ligand and receptor expression; PDGF signaling was essential for TGFβ-mediated migration.
Conclusions:
- TGFβ signaling is crucial for proper mesenchymal migration during dorsal vertebrae development.
- TGFβ acts on sclerotome to regulate PDGF ligand expression, which then acts paracrinely on adjacent mesenchyme.
- This TGFβ-PDGF axis mediates mesenchymal proliferation, migration, and differentiation, essential for forming dorsal vertebral structures.
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