Glial fibrillary acidic protein (GFAP) is one of the best markers for the activation of astrocytes (AS) following injury or stress in the central nervous system (CNS). The purpose of this study was to examine the expression of GFAP and 14-3-3ε in rat AS subjected to hypoxia. We established primary cultures of AS from cerebral cortex of neonatal Sprague-Dawley rats as a model of glucose deficiency and hypoxia/ischemia-reperfusion. We analyzed the activated astrocyte markers GFAP and 14-3-3ε by western blot analysis and found that both increased over time, starting at 4 h and reaching the highest level at 72 h, at the end of the experiment. GFAP and 14-3-3ε protein localization by double-labeling immunofluorescence showed elevated expression and co-localization in the cytoplasm of AS. GFAP and 14-3-3ε expression remained elevated in AS 72 h after stress conditions, which is possibly related to the excessive activation and dysfunction of the CNS in chronic injuries.

The technique of TRSP approach is safe, effective, and offers some advantages over the classic posterior, anterior, combined anterior-posterior approach for some specific highly unstable thoracolumbar fractures.

Osteosarcoma (OS) is a tumor with rapid progression, high metastatic potential and poor clinical prognosis. This study was aimed to investigate the function of miR-126 in OS cells. The miR-126 expression in OS cell lines and OS tissues were explored by qRT-PCR. Then, the effects of miR-126 on proliferation, cycle, migration, invasion, and transforming growth factor (TGF)-β1 induced epithelial to mesenchymal transition (EMT) were assessed. Predicted by TargetScan, one of target genes for miR-126 was verified by luciferase activity assay. Meantime, the mRNA and protein expressions of ZEB1 were assessed by qRT-PCR and Western blot assay. Subsequently, the effect of ZEB1 silence on miR-126 down-regulated cells was also evaluated. Finally, the expressions of key kinases involved in c-Jun N-terminal kinase (JNK) and Janus-activated kinase (JAK)-1/signal transducer and activator of transcription (STAT)-3 pathways were detected by Western blot analysis. Result showed that miR-126 was down-regulated in OS tissues and cell lines. Overexpression of miR-126 significantly inhibited cell proliferation, migration, invasion, and TGF-β1 induced EMT. The effect of miR-126 knockdown was just the opposite. ZEB1 was predicted and verified as a target gene of miR-126. Meantime, the influence of miR-126 knockdown was abrogated by ZEB1 silence. Additionally, the phosphorylation levels of c-Jun, JNK, JAK1, and STAT3 were down-regulated in miR-126 over-expressed cells, and the effect of miR-126 knockdown was reversed by ZEB1 silence. In conclusion, miR-126 inhibits proliferation, migration, invasion and EMT in OS by targeting ZEB1 through inactivation of JNK and JAK1/STAT3 pathways. J. Cell. Biochem. 118: 3765-3774, 2017. © 2017 Wiley Periodicals, Inc.