ABSTRACT
BACKGROUND: Melanoma is the most fatal form of skin cancer due to its rapid metastasis. Recently, several studies reported that selenium can induce apoptosis in melanoma cells. However, the precise mechanism remains to be elucidated. In this study, we investigated the effect of selenium on cell proliferation in murine melanoma and on tumor growth and metastasis in C57BL/6 mice. METHODS: Cell proliferation was measured by MTT assay in selenium-treated melanoma cells. Cell cycle distribution was analysized by staining DNA with propidum iodide (PI). mRNA and protein expression related to cell cycle arrest was measured by reverse transcription PCR and western blot. Tumor growth and metastasis was measured by in vivo model. RESULTS: Selenium was suppressed the proliferation of melanoma cells in a dose dependent manner. The growth inhibition of melanoma by selenium was associated with an arrest of cell cycle distribution at G0/G1 stage. The mRNA and protein level of CDK2/CDK4 was suppressed by treatment with selenium in a time-dependent manner. In vivo, tumor growth was not suppressed by selenium; however tumor metastasis was suppressed by selenium in mouse model. CONCLUSION: These results suggest that selenium might be a potent agent to inhibit proliferative activity of melanoma cells.
Subject(s)
Animals , Mice , Apoptosis , Blotting, Western , Cell Cycle , Cell Cycle Checkpoints , Cell Death , Cell Proliferation , DNA , Melanoma , Neoplasm Metastasis , Polymerase Chain Reaction , Reverse Transcription , RNA, Messenger , Selenium , Skin NeoplasmsABSTRACT
BACKGROUND: Microglial cells, major immune effector cells in the central nervous system, become activated in neurodegenerative disorders. Activated microglial cells produce proinflammatory mediators such as nitric oxide (NO), tumor necrosis factor-alpha and interleukin-1beta(IL-1beta). These proinflammatory mediators have been shown to be significantly increased in the neurodegenerative disorders such as Alzhimer's disease and Pakinson's disease. It was known that one of the neurodegeneration source is stress and it is important to elucidate mechanisms of the stress response for understanding the stress-related disorders and developing improved treatments. Because one of the neuropeptide which plays a main role in regulating the stress response is corticotropin- releasing hormone (CRH), we analyzed the regulation of NO release by CRH in BV2 murine microglial cell as macrophage in the brain. METHODS: First, we tested the CRH receptor expression in the mRNA levels by RT-PCR. To test the regulation of NO release by CRH, cells were treated with CRH and then NO release was measured by Griess reagent assay. RESULTS: Our study demonstrated that CRH receptor 1 was expressed in BV2 murine microglial cells and CRH treatment enhanced NO production. Furthermore, additive effects of lipopolysaccaride (LPS) and CRH were confirmed in NO production time dependantly. CONCLUSION: Taken together, these data indicated that CRH is an important mediator to regulate NO release on microglial cells in the brain during stress.
Subject(s)
Brain , Central Nervous System , Corticotropin-Releasing Hormone , Macrophages , Neurodegenerative Diseases , Neuropeptides , Nitric Oxide , Receptors, Corticotropin-Releasing Hormone , RNA, Messenger , Tumor Necrosis Factor-alphaABSTRACT
No abstract available.
Subject(s)
Cell Line , Cell Proliferation , Cytokines , Leukemia, Erythroblastic, AcuteABSTRACT
Several measurements were performed about 105 cases of normal stress A-P arthrographic findings in adult knee including discoid without tearing or osteoarthritis, those were selected from 166 cases examined arthrographicaliy under same technical condition due to suspicious internal derangement of the knee from October 1976 to March 1980. After stastistical analysis and comparative study about chondrai thickness, chondral index, meniscal size, meniscal index, intermeniscal distance, type of meniscus, communication between knee and proximal tibiofibular joint, following results were obtained. 1. Chondral thickness of normal articular cartilage was not related to joint size, but almost same value individually. Mean chondral thickness In P and P points was 2.90±0.63mm, 2.90±0.62mm, 2.93±0.64mm, 2.92±0.65mm in lateral, medial femoral condyle and lateral, medial tibial condyle in order. Age change was not seen statistically. 2. The size of meniscus was correlated nearly proportional with that of the joint. Mean lateral meniscus size (transverse meniscal length × meniscal thickness) was 12.55±2.50mm × 6.53±0.7mm in male and 10.13±2.25mm × 6.02±0.52mm in female. That of medial meniscus was 9.79+1.54mm × 5.85+ 0.45mm in male, and 7.72±1.64mm × 5.36±0.92mm in female. Age change was not seen statistically either. 3. Mean intermeniscal distance was 60.21x2.74mm in male, 53.34±3.31mm in female and occupied 83% in male, 82% in female of joint size each other. 4. In types of meniscus, normal type was 8.10%, infantile type dlscoid 12.4%, intermediate type 2.9%, primitive type 3.7% each other. 5. Communications between knee joint and proximal tibiofibular joint were seen in 24%.