Vascular Basement Membrane Fragmentation in Keloids and the Expression of Key Basement Membrane Component Genes
Yusaku Saijo1, Shizuko Ichinose1, Teruyuki Dohi1
1From the Department of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School Hospital, Tokyo, Japan.
Plastic and Reconstructive Surgery. Global Open
|December 24, 2024
Summary
Keloid scars show fragmented vascular basement membranes (VBMs), indicating increased vascular permeability. This supports the theory that abnormal VBM structure contributes to keloid formation and chronic inflammation.
Area of Science:
- Dermatology
- Cell Biology
- Pathology
Background:
- Keloids are abnormal scars resulting from dermal injury and chronic inflammation.
- Vascular hyperpermeability may drive inflammation by allowing immune cells and factors to enter tissues.
- The vascular basement membrane (VBM) acts as a barrier, and its integrity is crucial for regulating cell ingress.
Purpose of the Study:
- To investigate alterations in VBM structure in keloids.
- To examine the expression of VBM component genes in keloid endothelial cells.
Main Methods:
- Transmission electron microscopy (TEM) was used to analyze VBM thickness, continuity, and layering in 27 keloid and 27 normal skin samples.
- Differential gene expression of 222 VBM component genes was analyzed in endothelial cells from keloid and normal skin using microarray data.
Main Results:
- Keloid VBMs were significantly thinner (0.053 nm vs. 0.078 nm), less continuous (46% vs. 85%), and had fewer layers (1.2 vs. 2.4) compared to normal skin.
- Keloidal endothelial cells showed altered expression of VBM genes, with 22 downregulated (e.g., papilin, laminin-α5) and 28 upregulated (e.g., laminin-β1, laminin-γ1).
Conclusions:
- Vascular basement membranes are significantly fragmented in keloids.
- These structural VBM changes in keloids suggest that vascular hyperpermeability plays a role in their initiation and progression.
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