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Osteocyte-induced angiogenesis via VEGF-MAPK-dependent pathways in endothelial cells
Indira Prasadam1, Yinghong Zhou, Zhibin Du
1Institute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove Campus, Brisbane, QLD, 4059, Australia, i.prasadam@qut.edu.au.
Molecular and Cellular Biochemistry
|October 29, 2013
Summary
Osteocytes, bone cells, regulate blood vessel formation (angiogenesis) by secreting factors that activate endothelial cells. This involves vascular endothelial growth factor (VEGF) and MAPK-ERK signaling pathways, crucial for bone health.
Area of Science:
- Bone biology
- Cellular signaling
- Angiogenesis research
Background:
- Osteocytes are known regulators of bone remodeling, influencing osteoblasts and osteoclasts.
- The role of osteocytes in bone vascularization and angiogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the interaction between osteocytes and endothelial cells.
- To elucidate the molecular mechanisms by which osteocytes influence angiogenesis.
Main Methods:
- Co-culture of osteocyte (MLOY4) and endothelial (HUVEC) cell lines.
- Assessing endothelial cell migration, proliferation, and tube formation.
- Quantitative real-time PCR for angiogenesis-related genes.
- Western blotting to analyze VEGF and MAPK signaling pathways.
Main Results:
- Osteocyte-conditioned media promoted endothelial cell proliferation, migration, and tube formation.
- Osteocytes upregulated angiogenesis-related genes in endothelial cells.
- VEGF secreted by osteocytes activated VEGFR2-MAPK-ERK signaling in endothelial cells.
- Inhibition of VEGF or MAPK-ERK pathways blocked osteocyte-mediated angiogenesis.
Conclusions:
- Osteocytes play a significant role in regulating angiogenesis.
- Osteocyte-derived VEGF and activation of the MAPK-ERK pathway are key mechanisms in this process.
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