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Multiscale molecular profiling of pathological bone resolves sexually dimorphic control of extracellular matrix
Aikta Sharma1, Alice Goring1, Peter B Johnson2
1School of Biological Sciences, Highfield Campus, University of Southampton, Southampton SO17 1BJ, UK.
Disease Models & Mechanisms
|February 10, 2021
Summary
Vascular Endothelial Growth Factor (VEGF) deletion in bone cells causes sex-specific collagen defects, impacting bone quality. This study reveals how VEGF loss alters collagen structure and mineralization differently in males and females.
Area of Science:
- Biochemistry
- Biophysics
- Developmental Biology
Background:
- Collagen assembly is crucial for bone mineralization and mechanical strength.
- Pathological alterations in skeletal collagen configuration are not fully understood.
- Vascular Endothelial Growth Factor (VEGF) deletion in osteoblasts causes sex-specific extracellular matrix (ECM) changes.
Purpose of the Study:
- To investigate the sex-specific effects of VEGF deletion on collagen arrangement and ECM composition in bone.
- To understand how divergent ECM control contributes to phenotypic dimorphism in bone disorders.
Main Methods:
- Utilized murine osteocalcin-specific Vegf knockout (OcnVEGFKO) models.
- Employed multiscale analysis including polarization-resolved second-harmonic generation (p-SHG) microscopy and backscattered electron scanning electron microscopy.
- Applied Raman spectroscopy for molecular analysis of collagen and matrix components.
Main Results:
- VEGF loss reduced collagen fiber number and disrupted matrix organization in males.
- Localized divergence in collagen orientation was observed due to OcnVEGFKO.
- VEGF deletion impacted collagen proline/hydroxyproline content, stability, and matrix carbonation in a sex-specific manner.
Conclusions:
- Macromolecular imaging and spectroscopy are effective for detecting collagen and ECM alterations in pathological bone.
- Sex-specific genetic regulation of ECM composition and arrangement by VEGF is critical for bone health.
- Understanding these dimorphic pathways is vital for treating bone disorders with sex-specific manifestations.
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