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1.
Eur Rev Med Pharmacol Sci ; 18(18): 2720-86, 2014.
Article in English | MEDLINE | ID: mdl-25317809

ABSTRACT

OBJECTIVE: To investigate the fluctuation patterns of Th17 and IL-17 cytokines during acute skin graft rejection in mice. MATERIALS AND METHODS: Preparations for mouse skin transplantation model. At days 1, 3, 5, and 7 post-grafting, the number of Th17 cells in the spleens was quantified by flow cytometry (FCM); IL-17 mRNA expression in the spleens and the skin grafts were analyzed by semiquantitative RT-PCR. Serum IL-17 levels were determined by enzyme-labeled immunosorbent assay (ELISA). RESULTS: The number of Th17 cells in the spleens gradually increased and peaked at day 7 post-grafting. IL-17 mRNA expression in the skin was strongest at day 5 post-grafting. IL-17 levels in peripheral blood was highest at day 5 post-grafting. CONCLUSIONS: Acute rejection of allogeneic skin grafts in mice may correlate with the number of Th17 lymphocytes and the secretion of cytokine IL-17. Th17 cell count and IL-17 level may serve as important reference indices for early rejection reactions after skin grafting.


Subject(s)
Graft Rejection/metabolism , Interleukin-17/biosynthesis , Skin Transplantation/methods , Skin/metabolism , Th17 Cells/metabolism , Animals , Graft Rejection/immunology , Interleukin-17/immunology , Male , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Skin/immunology , Th17 Cells/immunology
2.
Cell Death Dis ; 5: e1129, 2014 Mar 20.
Article in English | MEDLINE | ID: mdl-24651432

ABSTRACT

Epithelial-to-mesenchymal transition (EMT) has an important role in invasion and metastasis of hepatocellular carcinoma (HCC). To explore the regulatory mechanism of atypical protein kinase C ι (aPKCι) signaling pathways to HCC development, and find an agent for targeted therapy for HCC, immortalized murine hepatocytes were employed to establish an EMT cell model of HCC, MMH-RT cells. Our study showed that EMT took place in MMH-R cells under the effect of transforming growth factor-ß1 (TGF-ß1) overexpressing aPKCι. Furthermore, we showed that the aPKCι blocking agent aurothiomalate (ATM) inhibited EMT and decreased invasion of hepatocytes. Moreover, ATM selectively inhibited proliferation of mesenchymal cells and HepG2 cells and induced apoptosis. However, ATM increased proliferation of epithelial cells and had little effect on apoptosis and invasion of epithelial cells. In conclusion, our result suggested that aPKCι could be an important bio-marker of tumor EMT, and used as an indicator of invasion and malignancy. ATM might be a promising agent for targeted treatment of HCC.


Subject(s)
Antineoplastic Agents/pharmacology , Biomarkers, Tumor/antagonists & inhibitors , Carcinoma, Hepatocellular/enzymology , Cell Movement/drug effects , Epithelial-Mesenchymal Transition/drug effects , Gold Sodium Thiomalate/pharmacology , Isoenzymes/antagonists & inhibitors , Liver Neoplasms/enzymology , Protein Kinase C/antagonists & inhibitors , Protein Kinase Inhibitors/pharmacology , Animals , Apoptosis/drug effects , Biomarkers, Tumor/metabolism , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/pathology , Cell Proliferation/drug effects , Cell Survival/drug effects , Dose-Response Relationship, Drug , Genes, ras , Hep G2 Cells , Humans , Isoenzymes/genetics , Isoenzymes/metabolism , Liver Neoplasms/genetics , Liver Neoplasms/pathology , Mice , Neoplasm Invasiveness , Protein Kinase C/genetics , Protein Kinase C/metabolism , Signal Transduction/drug effects , Time Factors , Transfection , Transforming Growth Factor beta1/metabolism
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