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Polyurethane (PU) is a class of polymers that have been applied for tissue-engineering scaffolds. Cross-linked poly(ester urethane) (CPU), synthesized with ferric catalyst in our laboratory, was modified by silk fibroin (SF) grafting using our aminolysis and glutaradehyde crosslinking method. The physical and chemical properties of the materials were investigated by scanning electron microscope (SEM), atomic force microscope (AFM) and tensile tester. The results showed that SF grafted CPU possessed good strain and strength (4.29 ± 0.18 MPa/382.38 ± 0.71%). Its surface chemistry and roughness were fine to well support the growth of bone marrow mesenchymal stem cells (BMSC). The cells were verified to maintain the pluripotency after they were cultured in vitro for 2 weeks, which supplied us a good technology to keep cell’s stemness but proliferate cell’s number. These results are valuable for us to further study esophageal tissue engineering with BMSC and polyurethane materials as the components. [ABSTRACT FROM AUTHOR]

Magnesium and Mg-based alloys are promising biomaterials for orthopedic implants because of their degradability, osteogenic effects, and biocompatibility. However, the drawbacks of these materials include high hydrogen gas production, unexpected corrosion resistance, and insufficient mechanical strength duration. Surface modification can protect these biomaterials and induce osteogenesis. In this work, a SrHPO 4 coating was developed for our patented biodegradable Mg–Nd–Zn–Zr alloy (abbr. JDBM) through a chemical deposition method. The coating was characterized by in vitro immersion, ion release, and cytotoxicity tests, which showed a slower corrosion behavior and excellent cell viability. RNA sequencing of MC3T3E1 cells treated with SrHPO 4 -coated JDBM ion release test extract showed increased Tlr4 , followed by the activation of the downstream PI3K/Akt signaling pathway, causing proliferation and growth of pre-osteoblasts. An intramedullary nail (IMN) was implanted in a femoral fracture rat model. Mechanical test, radiological and histological analysis suggested that SrHPO 4 -coated JDBM has superior mechanical properties, induces more bone formation, and decreases the degradation rate compared with uncoated JDBM and the administration of TLR4 inhibitor attenuated the new bone formation for fracture healing. SrHPO 4 is a promising coating for JDBM implants, particularly for long-bone fractures. • SrHPO 4 reduces the in vivo corrosion rate of Mg–Nd–Zn–Zr implants. • Release of Sr2+ and Mg2+ ions induces a biochemical response in rat femur fracture model. • Osteogenic response is stimulated by the TLR4/PI3K/Akt signaling pathway. • Improved mechanical stability and osteogenic induction enhances fracture healing. [ABSTRACT FROM AUTHOR]

The adverse effects of glucocorticoids (GCs) on bone marrow stromal stem cells (BMSCs) play an important role in steroid-induced osteonecrosis of the femoral head (ONFH). Our previous miRNA microarray analysis indicated that microRNA-224-5p (miR-224-5p) could be a potential regulator; however, the underlying mechanism remains unclear. In the present study, we demonstrated that miR-224-5p was upregulated in GC-treated BMSCs, and functional experiments revealed that miR-224-5p could suppress osteogenic but promote adipogenic differentiation of BMSCs. Smad4 was identified as a direct target gene of miR-224-5p, and the Smad4-Taz axis was confirmed as the regulatory pathway for adipo-osteogenic differentiation of BMSCs. Our in vivo experiments further confirmed that the miR-224-5p antagomir could alleviate the inhibitory effects of GCs and facilitate bone formation in steroid-induced ONFH models. Therefore, these findings provide insight into the function of miR-224-5p as a reciprocal regulator of the adipo-osteogenic differentiation of BMSCs, and it could serve as a novel therapeutic target for steroid-induced ONFH. • miR-224-5p serves as a reciprocal regulator of the adipo-osteogenic differentiation of BMSCs. • Smad4-TAZ axis is the intrinsic regulator of miR-224-5p in osteogenesis and adipogenesis. • Inhibition of miR-224-5p reduces the degree and incidence of steroid-induced ONFH. [ABSTRACT FROM AUTHOR]