ABSTRACT
@#As the key to regeneration of oral and maxillofacial tissues such as bone, dental pulp and skin, vascularization has always been the focus of tissue engineering. With the development of three-dimensional (3D) printing in tissue engineering, there are increasing ways to construct vascular structures. However, to achieve the objective of highly simulating vascular structure in morphology and function and promote tissue repair, it is still a major difficulty for 3D bioprinting to construct highly precise and biologically functional simulated vascular structures. This paper summarizes new progress of 3D printing vascular structure, expounds frontier biological manufacturing technologies of vascular and vascularized structure such as suspension printing, coaxial printing, 4D printing, and so on, analyzes its advantages and disadvantages, and discusses its development prospect, in order to provide reference for the application of 3D printing blood vessels in regeneration and repair of oral and maxillofacial tissues.
ABSTRACT
Human adipose-derived stem cells (hASCs) are a promising cell type for bone tissue regeneration. Circular RNAs (circRNAs) have been shown to play a critical role in regulating various cell differentiation and involve in mesenchymal stem cell osteogenesis. However, how circRNAs regulate hASCs in osteogenesis is still unclear. Herein, we found circ_0003204 was significantly downregulated during osteogenic differentiation of hASCs. Knockdown of circ_0003204 by siRNA or overexpression by lentivirus confirmed circ_0003204 could negatively regulate the osteogenic differentiation of hASCs. We performed dual-luciferase reporting assay and rescue experiments to verify circ_0003204 regulated osteogenic differentiation via sponging miR-370-3p. We predicted and confirmed that miR-370-3p had targets in the 3'-UTR of HDAC4 mRNA. The following rescue experiments indicated that circ_0003204 regulated the osteogenic differentiation of hASCs via miR-370-3p/HDAC4 axis. Subsequent in vivo experiments showed the silencing of circ_0003204 increased the bone formation and promoted the expression of osteogenic-related proteins in a mouse bone defect model, while overexpression of circ_0003204 inhibited bone defect repair. Our findings indicated that circ_0003204 might be a promising target to promote the efficacy of hASCs in repairing bone defects.