Search

Abstract Recent progress in additive manufacturing has enabled the application of stereolithography (SLA) in bioprinting to produce 3D biomimetic structures. Bioinks for SLA often require synthetic polymers as supplements to ensure the structural integrity of the printed cell‐laden constructs. High molecular weight (MW) poly(ethylene‐glycol)‐diacrylate (PEGDA) (MW ≥ 3400 Da) is commonly used to enhance the mechanical property of crosslinked hydrogels. However, the production of bioink with high MW PEGDA requires in‐house polymer synthesis or the acquisition of costly reagents, which may not be readily available in all laboratory settings. As an alternative to high MW PEGDA, this research investigated the use of poly(ethylene‐glycol)‐dimethacrylate (PEGDMA) (MW = 1000 Da) as a supplement of a bioink to enhance the mechanical properties of the SLA‐printed constructs. The successful demonstration showcases 1) the fabrication of 3D constructs with overhang and complex architecture, and 2) the cytocompatibility, with high cell viability of 71–87% over 6 days of culture, of the GelMA‐PEGDMA bioink to enable cell‐laden bioprinting. This study suggests PEGDMA as a viable supplement in the formulation of SLA bioink. The accessibility to PEGDMA will facilitate the advance in 3D bioprinting to fabricate complex bioinspired structures and tissue surrogates for biomedical applications.

Abstract The generation of structurally standardized human pluripotent stem cell (hPSC)‐derived neural embryonic tissues has the potential to model genetic and environmental mediators of early neurodevelopmental defects. Current neural patterning systems have so far focused on directing cell fate specification spatio‐temporally but not morphogenetic processes. Here, the formation of a structurally reproducible and highly‐organized neuroepithelium (NE) tissue is directed from hPSCs, which recapitulates morphogenetic cellular processes relevant to early neurulation. These include having a continuous, polarized epithelium and a distinct invagination‐like folding, where primitive ectodermal cells undergo E‐to‐N‐cadherin switching and apical constriction as they acquire a NE fate. This is accomplished by spatio‐temporal patterning of the mesoendoderm, which guides the development and self‐organization of the adjacent primitive ectoderm into the NE. It is uncovered that TGFβ signaling emanating from endodermal cells support tissue folding of the prospective NE. Evaluation of NE tissue structural dysmorphia, which is uniquely achievable in the model, enables the detection of apical constriction and cell adhesion dysfunctions in patient‐derived hPSCs as well as differentiating between different classes of neural tube defect‐inducing drugs.