ABSTRACT
OBJECTIVE: To investigate the role and regulate the target of miRNA-411 on spinal cord injury. MATERIALS AND METHODS: The microglia cultured in vitro was activated by lipopolysaccharide (LPS) to express the inflammatory phenotype. The inflammatory response through miRNA-411 transfection in microglia was measured to certain whether increased miRNA-411 suppressed interleukin-18 (IL-18) level to attenuate the inflammation amplification via downregulating JNK pathway. Furthermore, we established spinal cord injury (SCI) model in SD rats and further explored the glial inflammatory degree and neurological recovery following miRNA-411 treatment. Lastly, we estimated the hindlimbs function of SCI rats with miRNA-411 administration or not within four weeks at post-SCI. RESULTS: In vitro, miRNA-411 inhibited IL-18 expression and downregulated JNK pathway, along with that inflammatory microglia were declined. In SCI rats, we detected the decreased amounts of inflammatory microglia and reduction of the inflammatory factors after miRNA-411 treatment. IL-18 and JNK pathway was also restrained resulted from increased miRNA-411. In addition, apoptosis degree in injury site reduced and survived axons were relatively multiple in the miRNA-411 group compared with the SCI group. The Basso-Beattie-Bresnahan (BBB) locomotor scores of miRNA-411 treated rats were superior to those in rats with no treatment. CONCLUSIONS: MiRNA-411 increase ameliorates the inflammatory microglia-induced neurological lesion and promotes neural recovery by JNK pathway inhibition via negative targeting IL-18 in SCI.
Subject(s)
Apoptosis/physiology , Inflammation Mediators/metabolism , MicroRNAs/biosynthesis , Spinal Cord Injuries/metabolism , Spinal Cord Injuries/prevention & control , Animals , Animals, Newborn , Inflammation Mediators/antagonists & inhibitors , Locomotion/physiology , Male , Rats , Rats, Sprague-Dawley , Spinal Cord Injuries/pathologyABSTRACT
OBJECTIVE: This study was designed to investigate the specific mechanism underlying the regulatory effect of long noncoding ribonucleic acids (lncRNAs) MSTO2P on lung cancer (LCa) cell proliferation and autophagy via regulating enhancer of zeste homolog (EZH2) expression. PATIENTS AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to analyze the levels of MSTO2P and EZH2 in 40 pairs of LCa tissues and corresponding adjacent tissues, as well as in LCa cell lines (H1299, H23, A549) and human bronchial epithelial cells (BEAS-2B). Besides, the effect of MSTO2P on cell proliferation ability was detected by cell counting kit-8 (CCK-8) and plate cloning experiments. The interaction between MTS02P and EZH2 as well as their effects on cell autophagy ability were examined by qRT-PCR and Western blot. RESULTS: The qRT-PCR results showed that MSTO2P expression in LCa tissues was remarkably higher than that in adjacent tissues. Meanwhile, compared with human bronchial epithelial cells, the level of MSTO2P was remarkably up-regulated in LCa cells. After down-regulating MSTO2P, the cell proliferation ability was weakened, and the protein levels of autophagy-related genes including Agt5, LC-3I, and LC-3II were remarkably down-regulated. At the same time, EZH2 expression in LCa tissues was also remarkably up-regulated relative to adjacent tissues, and it was positively correlated with the expression of MSTO2P. In addition, after down-regulating MSTO2P, the EZH2 level was also remarkably reduced. Further experimental results revealed that EZH2 down-regulation could impair the cell proliferation ability and down-regulate the expressions of autophagy genes such as Agt5, LC-3I, and LC-3II. CONCLUSIONS: LncRNA MSTO2P promotes LCa cell proliferation and autophagy by up-regulating EZH2. Therefore, MSTO2P may be a potential therapeutic target for LCa.
Subject(s)
Enhancer of Zeste Homolog 2 Protein/genetics , Gene Expression Regulation, Neoplastic , Lung Neoplasms/genetics , RNA, Long Noncoding/metabolism , Autophagy/genetics , Cell Line, Tumor , Cell Proliferation/genetics , Down-Regulation , Gene Knockdown Techniques , Humans , Lung/pathology , Lung/surgery , Lung Neoplasms/pathology , Lung Neoplasms/surgery , Pneumonectomy , RNA, Long Noncoding/genetics , RNA, Small Interfering/metabolism , Up-RegulationABSTRACT
The initial growth stage of the single-crystalline Sb and Co nanowires with preferential orientation was studied, which were synthesized in porous anodic alumina membranes by the pulsed electrodeposition technique. It was revealed that the initial growth of the nanowires is a three-dimensional nucleation process, and then gradually transforms to two-dimensional growth via progressive nucleation mechanism, which resulting in a structure transition from polycrystalline to single crystalline. The competition among the nuclei inside the nanoscaled-confined channel and the growth kinetics is responsible for the structure transition of the initial grown nanowires.
