Small-diameter tissue-engineered vascular grafts are urgently needed for clinic arterial substitute. To simulate the structures and functions of natural blood vessels, we designed a novel triple-layer poly(ε-caprolactone) (PCL) fibrous vascular graft by combining E-jet 3D printing and electrospinning techniques. The resultant vascular graft consisted of an interior layer comprising 3D-printed highly aligned strong fibers, a middle layer made by electrospun densely fibers, and an exterior structure composed of mixed fibers fabricated by co-electrospraying. The biocompatible triple-layer graft was used for in vivo implantation, and results demonstrated that the longitudinally-aligned fibers within the lumen of the graft could enhance the proliferation and migration of endothelial cells, while maintained good mechanical properties. The exterior layer provided a pathway that encouraged cells to migrate into the scaffold after implantation. This experimental graft overcame the limitations of conventionally electrospun vascular grafts of inadequate porosity and lowly cell penetration. The unique structure of the triple-layer vascular graft promoted cell growth and infiltration in vivo, thus provided an encouraging substitute for in situ tissue engineering.
BackgroundSkeletal muscle tissue engineering often involves the prefabrication of muscle tissues in vitro by differentiation and maturation of muscle precursor cells on a platform which provides an environment that facilitates the myogenic differentiation of the seeded cells.MethodsPoly lactic-co-glycolic acid (PLGA) 3D printed scaffolds, which simulate the highly complex structure of extracellular matrix (ECM), were fabricated by E-jet 3D printing in this study. The scaffolds were used as platforms, providing environment that aids in growth, differentiation and other properties of C2C12 myoblast cells.ResultsThe C2C12 myoblast cells grown on the PLGA 3D printed platforms had enhanced cell adhesion and proliferation. Moreover, the platforms were able to induce myogenic differentiation of the myoblast cells by promoting the formation of myotubes and up-regulating the expressions of myogenic genes (MyHC and MyOG).ConclusionThe fabricated 3D printed platforms have excellent biocompatibility, thereby can potentially be used as functional cell culture platforms in skeletal tissue engineering and regeneration.
Background
Long noncoding RNAs (lncRNAs) have been identified as regulators of a number of developmental and tumorigenic processes. However, the functions of most lncRNAs in glioma remain unknown and the mechanisms governing the proliferation of tumor cells remain poorly defined.
Methods
Both
in vitro
and
in vivo
assays were performed to investigate the roles of lncRNAs in the pathophysiology of gliomas. lncRNA arrays were used to identify differentially expressed lncRNAs. Subcutaneous tumor formation and a brain orthotopic tumor model in nude mice were used to investigate the functions of lncRNAs
in vivo
. The
in vitro
functions of lncRNAs were analyzed by fluorescence-activated cell sorting, colony formation, and western blot analyses. RNA fluorescence
in situ
hybridization and immunoprecipitation were used to explore the underlying mechanisms.
Findings
Here, we describe the newly discovered noncoding RNA RP11-732M18.3, which is highly overexpressed in glioma cells and interacts with 14-3-3β/α to promote glioma growth, acting as an oncogene. Overexpression of lncRNA RP11-732 M18.3 was associated with the proliferation of glioma cells and tumor growth
in vitro
and
in vivo
. Remarkably, lncRNA RP11-732M18.3 promoted cell proliferation and G1/S cell cycle transition. lncRNA RP11-732M18.3 is predominately localized in the cytoplasm. Mechanistically, the interaction of lncRNA RP11-732M18.3 with 14-3-3β/α increases the degradation of the p21 protein. lncRNA RP11-732M18.3 promoted the recruitment of ubiquitin-conjugating enzyme E2 E1 to 14-3-3β/α and the binding of 14-3-3β/α with ubiquitin-conjugating enzyme E2 E1 (UBE2E1) promoted the degradation of p21.
Interpretation
Overall these data demonstrated that lncRNA RP11-732M18.3 regulates glioma growth through a newly described lncRNA-protein interaction mechanism. The inhibition of lncRNA RP11-732M18.3 could provide a novel therapeutic target for glioma treatment.
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