Superhydrophobic fluoride conversion coating on bioresorbable magnesium alloy——fabrication,characterization,degradation and cytocompatibility with BMSCs

A micro-nano structure CaF_(2)chemical conversion layer was prepared on fluoride-treated AZ31 alloy,then the composite fluoride conversion film(CaF_(2)/MgF_(2))was modified by stearic acid(SA)and fabricated a superhydrophobic surface.The fluoride-treated magnesium,fluoride conversion film and superhydrophobic coating were characterized by SEM,EDS,XRD and FTIR.The properties of coatings1 adhesion and corrosion resistance were evaluated via tape test and electrochemical measurement.The cytocompatibility of the MgF_(2),CaF_(2)and superhydrophobic CaF_(2)/SA surface was investigated with bone marrow-derived mesenchymal stem cells(BMSCs)by direct culture for 24 h.The results showed that the superhydrophobic fluoride conversion coating composed of inner MgF_(2)layer and the outer CaF_(2)/SA composite layer had an average water contact angle of 152°.SA infiltrated into the micro-nano structure CaF_(2)layer and formed a strong adhesion with CaF_(2)layer.Furthermore,the super-hydrophobic coating showed higher barrier properties and corrosion resistance compared with the fluoride conversion film and fluoride-treated AZ31 alloy.The BMSC adhesion test results demonstrated MgF_(2)CaF_(2)and CaF_(2)/SA coatings were all nontoxic to BMSC.At the condition of in direct contact with cells,MgF_(2)showed higher cell density and enhanced the BMSCs proliferation,while CaF_(2)and CaF_(2)/SA coating showed no statistically difference in cell density compared with glass reference but the CaF_(2)and CaF_(2)/SA coating were not conducive to BMSCs adhesion.

RP11-40C6.2 Inactivates Hippo Signaling by Attenuating YAP1 Ubiquitylation in Hepatitis B Virus-associated Hepatocellular Carcinoma

Background and Aims:Chronic hepatitis caused by hepatitis B virus(HBV)infection is a leading cause of hepatocellular carcinoma(HCC).We investigated the roles of oncogenic HBV infection-associated long noncoding RNAs in HCC.Methods:Bioinformatics analysis of data from the Cancer Genome Atlas(TCGA)was performed to screen potential oncogenic HBV-related lncRNAs.Next,we assessed their expression in clinical samples and investigated their correlation with clinical characteristics.The detailed oncogenic effects were analyzed by performing in vitro and in vivo studies.Results:RP11-40C6.2,an HBV infection-related lncRNA,was identified by analysis of the TCGA–Liver Hepatocellular Carcinoma database.Gene Set Enrichment Analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analysis of differentially expressed genes revealed a strong association of RP11-40C6.2 with the Hippo signaling pathway.RP11-40C6.2 was overexpressed in HCC patients with HBV infection compared to those without HBV infection.RP11-40C6.2 transcription showed a positive association with HBV-X protein(HBx),but not HBV core protein(HBc)expression,both of which are carcinogenic proteins.Luciferase gene reporter and ChIP assays revealed that YAP1/TAZ/TEADs complex enhanced RP11-40C6.2 transcription by binding to its promoter area.RP11-40C6.2 showed oncogenic characteristics in HCC cell lines and in animal models that were mediated via activation of YAP1.In vitro ubiquitylation assay revealed that RP11-40C6.2 can promote the stabilization of YAP1 by stopping phosphorylation at its s127 residue and further stopping its degradation through binding to 14-3-3.Conclusions:RP11-40C6.2 is an HBV infection-related lncRNA that exerts its oncogenic effects by targeting the Hippo signaling pathway.