Inflammation mediated by the peripheral infiltration of inflammatory cells plays an important role in intracerebral hemorrhage (ICH) induced secondary injury. Previous studies have indicated that regulatory T lymphocytes (Tregs) might reduce ICH-induced inflammation, but the precise mechanisms that contribute to ICH-induced inflammatory injury remain unclear. Our results show that the number of Tregs in the brain increases after ICH. Inducing Tregs deletion using a CD25 antibody or Foxp3 DTR -mice increased neurological deficient scores (NDS), the level of inflammatory factors, hematoma volumes, and neuronal degeneration. Meanwhile, boosting Tregs using a CD28 super-agonist antibody reduced the inflammatory injury. Furthermore, Tregs depletion shifted microglia/macrophage polarization toward the M1 phenotype while boosting Tregs shifted this transition toward the M2 phenotype. In vitro, a transwell co-culture model of microglia and Tregs indicated that Tregs changed the polarization of microglia, decreased the expression of MHC-II, IL-6, and TNF-a and increased CD206 expression. IL-10 originating from Tregs mediated the microglia polarization by increasing the expression of Glycogen Synthase Kinase 3 beta (GSK3b), which phosphorylates and inactivates Phosphatase and Tensin homologue (PTEN) in microglia, TGF-b did not participate in this conversion. Thus, Tregs ameliorated ICH-induced inflammatory injury by modulating microglia/macrophage polarization toward the M2 phenotype through the IL-10/GSK3b/PTEN axis.
Background Hepatocellular carcinoma (HCC) is a common malignancy with high morbidity. The current study aimed to explore the molecular mechanism of lncRNA SLC16A1‐AS1 in the tumorigenesis of HCC. Material and methods The expression of SLC16A1‐AS1 and miR‐411 was examined in clinical HCC tissues. HCC cell lines Hep3B and Huh‐7 were employed and transfected with si‐SLC16A1‐AS1. The correlation between SLC16A1‐AS1 and miR‐411 was verified by luciferase reporter assay. Cell viability was detected by CCK‐8 assay. Cell migration and invasion capacity were examined by transwell assay. The protein level of MITD1 was analyzed by western blotting. Results The expression of SLC16A1‐AS1 markedly increased in HCC tissues and cell lines. Subsequent studies identified SLC16A1‐AS1 as a downstream target of miR‐411. In addition, SLC16A1‐AS1 knockdown and miR‐411 overexpression significantly stagnated the progression of HCC cells. SLC16A1‐AS1 knockdown also downregulated MITD1 levels. Conclusion Our findings showed that SLC16A1‐AS1 was overexpressed in HCC cells and tissues. SLC16A1‐AS1 promoted the malignant characteristics of HCC cells and acted as an oncogene. Its regulatory effect may be associated with miR‐411/MITD1 axis. Therefore, SLC16A1‐AS1 has the potential to be used as a biomarker or therapeutic target for the treatment of HCC.
Background: Hepatocellular carcinoma (HCC) is a common malignancy with high morbidity. The current study aimed to explore the molecular mechannism of lncRNA SLC16A1-AS1 in the tumorigenesis of HCC.Material and Methods: The expression of SLC16A1-AS1 and miR-411 were examined in clinical HCC tissues. HCC cell lines Hep3B and Huh-7 were employed and transfected with si-SLC16A1-AS1. The correlation between SLC16A1-AS1 and miR-411 was verified by luciferase reporter assay. Cell viability was detected by CCK-8 assay. Cell migration and invasion capacity were examined by transwell assay. The protein level of MITD1 was analyzed by western blotting.Results: The expression of SLC16A1-AS1 markedly increased in HCC tissues and cell lines. Subsequent studies identified SLC16A1-AS1 as a downstream target of miR-411. In addition, SLC16A1-AS1 knockdown and miR-411 overexpression significantly stagnated progression of HCC cells. SLC16A1-AS1 knockdown also downregulated MITD1 levels. Conclusion: Our findings showed that SLC16A1-AS1 was overexpressed in HCC cells and tissues. SLC16A1-AS1 promoted the malignant characteristics of HCC cells and acted as an oncogene. Its regulatory effect may be associated with miR-411/MITD1 axis. Therefore, SLC16A1-AS1 has a potential be used as a biomarker or therapeutic target for the treatment of HCC.
In allusion to limitations of traditional data processing technology in big data processing, big data processing system architecture based on hadoop is designed, using the characteristics of quantification, unstructured and dynamic of cloud computing.It uses HDFS be responsible for big data storage, and uses MapReduce be responsible for big data calculation and uses Hbase as unstructured data storage database, at the same time a system of storage and cloud computing security model are designed, in order to implement efficient storage, management, and retrieval of data,thus it can save construction cost, and guarantee system stability, reliability and security.
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