The effect of FGF-1 loaded alginate microbeads on neovascularization and adipogenesis in a vascular pedicle model of adipose tissue engineering.
Engineered vascularized adipose tissue could serve as an alternative to traditional tissue reconstruction procedures. Adipose formation occurs in a coordinated fashion with neovascularization. Previous studies have shown that extracellular matrix-based materials supplemented with factors that stimulate neovascularization promote adipogenesis in a number of animal models. The present study examines the ability of fibroblast growth factor (FGF-1) delivered from alginate microbeads to induce neovascularization and adipogenesis in type I collagen gels in a vascular pedicle model of adipose tissue engineering. FGF-1 loaded microbeads stimulated greater vascular network formation in an in vitro 3D co-culture model than a single bolus of FGF-1. In in vivo studies, FGF-1 loaded beads suspended in collagen and implanted in a chamber surrounding the exposed femoral pedicle of a rat resulted in a significant increase in vascular density at 1 and 6 weeks in comparison to bolus administration of FGF-1. Staining for smooth muscle actin showed that over 48% of vessels had associated mural cells. While an increase in neovascularization was achieved, there was less than 3% adipose under any condition. These results show that delivery of FGF-1 from alginate beads stimulated a more persistent neovascularization response than bolus FGF-1 both in vitro and in vivo. However, unlike previous studies, this increased neovascularization did not result in adipogenesis. Future studies need to provide a better understanding of the relationship between neovascularization and adipogenesis in order to design advanced tissue engineering therapies.
Moya
Monica L
ML
Pritzker Institute of Biomedical Science & Engineering and Department of Biomedical Engineering, Illinois Institute of Technology, 3255 South Dearborn St, Chicago, IL 60616, USA.
Cheng
Ming-Huei
MH
Huang
Jung-Ju
JJ
Francis-Sedlak
Megan E
ME
Kao
Shu-Wei
SW
Opara
Emmanuel C
EC
Brey
Eric M
EM
D000199:Actins / Q000378:metabolism; D050156:Adipogenesis / Q000187:drug effects*; D000273:Adipose Tissue / Q000187:drug effects*; D000464:Alginates / Q000494:pharmacology*; D000818:Animals; D001808:Blood Vessels / Q000187:drug effects; D018920:Coculture Techniques; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D016220:Fibroblast Growth Factor 1 / Q000494:pharmacology*; D020723:Glucuronic Acid / Q000494:pharmacology; D006603:Hexuronic Acids / Q000494:pharmacology; D006801:Humans; D008863:Microspheres; D008954:Models, Biological; D018919:Neovascularization, Physiologic / Q000187:drug effects*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D023822:Tissue Engineering / Q000379:methods*
D000199:Actins; D000464:Alginates; D016220:Fibroblast Growth Factor 1; D020723:Glucuronic Acid; D006603:Hexuronic Acids; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C498862:Acta2 protein, rat