An investigation to optimize angiogenesis within potential dermal replacements.
BACKGROUND
Acute and chronic wounds are costly and invariably expose significant structures. Surgical reconstruction causes donor-site morbidity, scarring, and the need for intensive care. Reconstruction using an artificial dermis avoids donor sites, but available collagen-based solutions are susceptible to poor take. Using an in vitro angiogenic assay, the authors investigated dermal matrices for potential inclusion in a second-generation proangiogenic synthetic dermal replacement.


METHODS
Human placental endothelial cells were cocultured on Cytodex beads (Pharmacia Biotech) and plated in eight different extracellular matrix gels (collagen, fibrin, four glycosaminoglycans, vitronectin, and fibronectin), with or without stimulation from two soluble angiogenic factors. Three different cell lines were used, with 30 beads per condition. Cellular invasion into gels was calculated using Sigma Scan computer software, and statistical comparisons were made.


RESULTS
The authors found that fibrin provided greatest stimulus for endothelial invasion, with invasion in fibrin inhibited by collagen in a concentration-dependent fashion. Invasion by alternative extracellular matrix components and soluble angiogenic factors was far less than that in fibrin.


CONCLUSIONS
The authors identified that extracellular matrices can provide greater angiogenic potential than soluble angiogenic factors. Fibrin provided a better proangiogenic scaffold than collagen. This could well be used to encourage blood vessel ingress and eventual take of a second-generation proangiogenic synthetic dermal replacement.
Potter
Matthew J
MJ
RAFT Institute, Mount Vernon Hospital, London, United Kingdom. mattpotters@hotmail.com
Linge
Claire
C
Cussons
Paul
P
Dye
Julian F
JF
Sanders
Roy
R
D043925:Angiogenesis Inducing Agents / Q000494:pharmacology; D018929:Cell Culture Techniques / Q000295:instrumentation / Q000379:methods; D002465:Cell Movement / Q000187:drug effects; D002809:Chondroitin Sulfates; D003094:Collagen; D003470:Culture Media; D003871:Dermatan Sulfate; D042783:Endothelial Cells / Q000166:cytology* / Q000187:drug effects; D004730:Endothelium, Vascular / Q000166:cytology*; D005109:Extracellular Matrix / Q000502:physiology*; D005260:Female; D005337:Fibrin; D005353:Fibronectins; D005782:Gels; D006025:Glycosaminoglycans; D006801:Humans; D008863:Microspheres; D018919:Neovascularization, Physiologic / Q000187:drug effects; D010920:Placenta / Q000098:blood supply; D011247:Pregnancy; D017768:Skin, Artificial; D042461:Vascular Endothelial Growth Factor A / Q000494:pharmacology; D019096:Vitronectin
D043925:Angiogenesis Inducing Agents; D003470:Culture Media; D005353:Fibronectins; D005782:Gels; D006025:Glycosaminoglycans; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D019096:Vitronectin; D003871:Dermatan Sulfate; D005337:Fibrin; D002809:Chondroitin Sulfates; D003094:Collagen