Tissue engineering. Part A
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3D bioprinting is an additive manufacturing technique that recapitulates the native architecture of tissues. This is accomplished through the precise deposition of cell-containing bioinks. The spatiotemporal control over bioink deposition permits for improved communication between cells and the extracellular matrix, facilitates fabrication of anatomically and physiologically relevant structures. ⋯ Graphical abstract [Figure: see text] Impact statement Extrusion-based 3D bioprinting is an emerging additive manufacturing approach for fabricating cell-laden tissue engineered constructs. This review critically evaluates bioink design criteria to fabricate complex tissue constructs. Specifically, pre- and post-printing evaluation approaches are described, as well as new research directions in the field of bioink development and functional bioprinting are highlighted.
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The aim of this study is to investigate the efficacy and the effect of the dosage of the slow-released Escherichia coli-derived recombinant human bone morphogenetic protein 2 (ErhBMP-2) functionalized β-tricalcium phosphate (β-TCP) in repairing critical-sized bone defects. The functionalization was implemented by modifying the surface of β-TCP with biomimetic calcium phosphate coating with or without ErhBMP-2. Critical-sized calvarial defects were created in rats and filled with ErhBMP-2 functionalized β-TCP loaded with gradient doses of ErhBMP-2 (0, 50, 100, 150, 200, and 300 μg/g). ⋯ To develop a commercial product with more effective cost, Escherichia coli-derived rhBMP-2 (ErhBMP-2) has been produced and evaluated as an alternative to the mammalian-derived rhBMP-2. In this study, we prepared gradient ErhBMP-2 functionalized β-tricalcium phosphate (β-TCP) with biomimetic calcium phosphate coating and investigate their efficacy and dose effects. We revealed the dose effects of the slow-released ErhBMP-2 and demonstrated that ErhBMP-2 functionalized β-TCP could be a promising bone substitute for bone regeneration in clinical settings.
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Transplanted bone marrow mononuclear cells (BMC) support the healing of large bone defects. Neutralization of microRNA (MiR) that negatively affects key processes of the reparative response in BMC might help to further improve the beneficial effect of transplanted BMC in bone healing. ⋯ Ultimate load as well as osseous integration of the β-TCP-scaffolds were significantly improved in the antiMiR-335 group compared to the control group after 8 weeks, whereas neutralization of antiMiR-92A lead to an improvement of early vascularization after 1 week, but not to enhanced bone healing after 8 weeks. We demonstrated that the targeted inhibition of MiRs in transplanted BMC is a new approach that enhances BMC-supported bone healing.
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Articular cartilage has poor capability of regeneration due to the avascular surrounding and low metabolic activity. Kartogenin (KGN), an emerging nonprotein heterocyclic compound, was screened to stimulate chondrogenic differentiation of bone mesenchymal stem cells (BMSCs). Coculturing BMSCs and chondrocytes was reported to overcome the shortcomings of forming fibroblastic and hypertrophic cartilages. ⋯ The complexes compounding KGN, BMSCs, and chondrocytes (at an optimal ratio in the in vitro experiment) were transplanted into rat models to evaluate the repair effects. Our results suggested that the interaction between BMSCs and chondrocytes can substitute the use of growth factors to some degree and indicated the role of KGN in chondrogenesis induction. Besides, it is the first time (to our knowledge) that the expression of lubricin was found to be delayed in the coculture of mixed cells comparing with GAGs and COL II, which could be significant in cartilage tissue engineering.
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Hypertrophic scar (HS) is a dermal fibroproliferative disease characterized by fibroblast over-proliferation, overproduction, and deposition of the extracellular matrix. Growing evidence demonstrated that adipose-derived stem cells (ASCs) secrete a plethora of trophic and antifibrotic factors, which suppress inflammation and ameliorate fibrosis of different tissues. However, few studies investigate their effect on repressing HS activity. ⋯ This study demonstrated that coculture of HSFs with ASCs not only inhibited proliferation, migration, and contractility of HSFs but also decreased the expression levels of HSF-related or TGF-β1-induced molecules. Additionally, the antifibrotic effect on HSFs was likely mediated by the inhibition of multiple intracellular signaling. The results of this study suggest the therapeutic potential of ASCs for HS treatment, which is worth of further investigation.