Tenascin‐c is an extracellular matrix glycoprotein, the expression of which relates to the progression of atherosclerosis, myocardial infarction and heart failure. Annexin II acts as a cell surface receptor of tenascin‐c. This study aimed to delineate the role of tenascin‐c and annexin II in macrophages presented in atherosclerotic plaque. Animal models with atherosclerotic lesions were established using ApoE‐KO mice fed with high‐cholesterol diet. The expression of tenascin‐c and annexin II in atherosclerotic lesions was determined by qRT‐PCR, Western blot and immunohistochemistry analysis. Raw 264.7 macrophages and human primary macrophages were exposed to 5, 10 and 15 μg/ml tenascin‐c for 12 hrs. Cell migration as well as the proangiogenic ability of macrophages was examined. Additionally, annexin II expression was delineated in raw 264.7 macrophages under normal condition (20% O2) for 12 hrs or hypoxic condition (1% O2) for 6–12 hrs. The expression of tenascin‐c and annexin II was markedly augmented in lesion aorta. Tenascin‐c positively regulated macrophage migration, which was dependent on the expression of annexin II in macrophages. VEGF release from macrophages and endothelial tube induction by macrophage were boosted by tenascin‐c and attenuated by annexin II blocking. Furthermore, tenascin‐c activated Akt/NF‐κB and ERK signalling through annexin II. Lastly, hypoxia conditioning remarkably facilitates annexin II expression in macrophages through hypoxia‐inducible factor (HIF)‐1α but not HIF‐2α. In conclusion, tenascin‐c promoted macrophage migration and VEGF expression through annexin II, the expression of which was modulated by HIF‐1α.
The pullout process of graphene from an epoxy/graphene composite filled with a carbon nanotube (CNT) was simulated by molecular dynamics simulations. The interaction energy and the interfacial adhesion energy were calculated to analyze the effect of CNT addition on the interfacial adhesion between the graphene and the epoxy matrix, with varying CNT radii, distances between the CNT and the graphene sheet, CNT axial directions, and the number of CNT walls. Generally, the addition of a CNT strengthens the interfacial adhesion between the graphene and the polymer matrix. Firstly, a larger CNT radius induces a stronger interfacial adhesion of graphene with the matrix. Secondly, when the CNT is farther away from the graphene sheet, the interfacial adhesion of graphene with the matrix becomes weaker. Thirdly, the CNT axial direction has little effect on the interfacial adhesion of graphene in the equilibrium structure. However, it plays an important role in the graphene pullout process. Finally, compared with a single-walled CNT, the interfacial adhesion between graphene and the matrix is stronger when a double-walled CNT is added to the matrix.
BackgroundThe mechanisms of lipid raft regulation by microRNAs in breast cancer are not fully understood. This work focused on the evaluation and identification of miR-3908, which may be a potential biomarker related to the migration of breast cancer cells, and elucidates lipid-raft-regulating cell migration in breast cancer.MethodsTo confirm the prediction that miR-3908 is matched with AdipoR1, we used 3’-UTR luciferase activity of AdipoR1 to assess this. Then, human breast cancer cell line MCF-7 was cultured in the absence or presence of the mimics or inhibitors of miR-3908, after which the biological functions of MCF-7 cells were analyzed. The protein expression of AdipoR1, AMPK, and SIRT-1 were examined. The interaction between AdipoR1 and Flotillin-1, or its effects on lipid rafts on regulating cell migration of MCF-7, was also investigated.ResultsAdipoR1 is a direct target of miR-3908. miR-3908 suppresses the expression of AdipoR1 and its downstream pathway genes, including AMPK, p-AMPK, and SIRT-1. miR-3908 enhances the process of breast cancer cell clonogenicity. miR-3908 exerts its effects on the proliferation and migration of MCF-7 cells, which are mediated by lipid rafts regulating AdipoR1’s ability to bind Flotillin-1.ConclusionsmiR-3908 is a crucial mediator of the migration process in breast cancer cells. Lipid rafts regulate the interactions between AdipoR1 and Flotillin-1 and then the migration process associated with miR-3908 in MCF-7 cells. Our findings suggest that targeting miR-3908 and the lipid raft, may be a promising strategy for the treatment and prevention of breast cancer.
The low-temperature annealing process has a critical impact on the electrical performance of thin-film transistors (TFTs). This paper reports significant performance enhancements of TFTs using a femtosecond laser pre-annealing (FLA)-based preparation method. The solution-processed In2O3 films were fabricated by FLA at various laser irradiation times and then annealed on a hot-plate at 230 ℃. When the FLA time was set to 30 s, the device exhibited high saturation mobility of 10.03 ± 0.64 cm 2 /Vs, Ion/Ioff of 3.4 × 10 5 , low VTH of 0.14 ± 0.64 V, and small SS of 1.44 ± 0.37 V/dec. The FLA process improved the formation of M-O lattices effectively, which led to an improvement in mobility. Furthermore, the gate-bias-stress stability and time-dependent environmental stability were improved considerably by the FLA process. These results show that high-performance In2O3 TFTs can be prepared at low temperatures using FLA-centered annealing technology. This work suggests that the FLA preparation method has tremendous potential for the fabrication of low-cost, high performance, and flexible TFT devices.INDEX TERMS In2O3, thin-film transistors, solution process, femtosecond laser, low-temperature, annealing process.
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