Pro-angiogenic CD14(++) CD16(+) CD163(+) monocytes accelerate the in vitro endothelialization of soft hydrophobic poly (n-butyl acrylate) networks.
As the majority of the polymers used as cardiovascular grafts so far do not match the elasticity of human arteries (100-1000kPa) and the required endothelialization, a multifunctional material approach is needed to allow the adjustment of the mechanical properties while at the same time exhibiting a haemocompatible surface. Recently soft poly(n-butyl acrylate) networks (cPnBA) with adjustable mechanical properties were introduced as candidate materials with a surface that can be endothelialized. In this study, angiogenically stimulated intermediate CD163(+) monocytes/macrophages (aMO2) were utilized as a cellular cytokine release system to realize the functional endothelialization of the hydrophobic cPnBA surface. We investigated the influence of co-cultured aMO2 on the morphology, density and cytokine secretion of human umbilical venous endothelial cells (HUVEC) seeded on cPnBA with an elastic modulus of around 250kPa (cPnBA0250). A functional confluent HUVEC monolayer could be developed in the co-culture within 3days. In contrast, the HUVEC in the monoculture exhibited stress fibres, broadened marginal filament bands and significantly more and larger cell-free areas in the monolayer, indicating incomplete cell-substrate binding. Remarkably, a functional confluent monolayer formation could only be achieved in co-cultures; it did not develop with the sole supplementation of recombinant VEGF-A(165) to the HUVEC monocultures (unpublished data). The study demonstrated the multifunctional potential of cPnBA in combination with aMO2 as a cellular cytokine release system, adapting their secretion to the demand of HUVEC. In this way, a functional confluent monolayer could be generated within 3days.
Center for Biomaterial Development and Berlin-Brandenburg Centre for Regenerative Therapies, Institute of Polymer Research, Helmholtz-Zentrum Geesthacht, Teltow, Germany.
Anke
A
Mayer
Toralf
T
Roch
Karl
K
Kratz
Andreas
A
Lendlein
Friedrich
F
Jung
D000179:Acrylates / Q000494:pharmacology*; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D002478:Cells, Cultured; D018920:Coculture Techniques; D005260:Female; D058851:GPI-Linked Proteins; D061307:Human Umbilical Vein Endothelial Cells / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D057927:Hydrophobic and Hydrophilic Interactions; D018950:Lipopolysaccharide Receptors; D008264:Macrophages / Q000166:cytology / Q000378:metabolism; D008297:Male; D009000:Monocytes / Q000166:cytology / Q000378:metabolism*; D018919:Neovascularization, Physiologic / Q000187:drug effects*; D011956:Receptors, Cell Surface; D017452:Receptors, IgG; D011994:Recombinant Proteins / Q000494:pharmacology; D042461:Vascular Endothelial Growth Factor A / Q000494:pharmacology; D000098902:CD163 Antigen
D000179:Acrylates; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000098902:CD163 Antigen; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D018950:Lipopolysaccharide Receptors; D011956:Receptors, Cell Surface; D017452:Receptors, IgG; D011994:Recombinant Proteins; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A