RESUMEN
BACKGROUND: During electricity generation of nuclear power plant, heat energy cannot be completely converted into electrical energy, and a part of it is lost in the form of thermal discharge into the environment. The thermal discharge is harmful to flora and fauna leading to environmental deterioration, biological diversity decline, and even biological extinction. RESULTS: The present study investigated the influence of thermal discharge from a nuclear power plant on the growth and development of Pacific oyster Crassostrea gigas which is widely used as bio indicator to monitor environmental changes. The growth of soft part and the gonad development of oysters were inhibited due to thermal discharge. During winter season, temperature elevation caused by thermal discharge promoted the growth of oyster shells. During summer season, the growth rate of oysters in thermal discharge area was significantly lower than that of the natural sea area. CONCLUSIONS: The results of this study provided a better understanding of assessing the impact of thermal discharge on the marine ecological environment and mariculture industry. It also provided a scientific basis for defining a safe zone for aquaculture in the vicinity of nuclear power plants.
Asunto(s)
Crassostrea/crecimiento & desarrollo , Calor/efectos adversos , Plantas de Energía Nuclear , Agua/análisis , Animales , Estrés FisiológicoRESUMEN
Osteoarthritis (OA) is characterized by progressive destruction of articular cartilage, resulting in significant disability. Chondrocytes present in various types of cartilage and are responsible for the growth and maintenance of the tissue. Over-proliferation of human chondrocytes may contributes to OA pathological process. Previously, we revealed that miR-127-5p could inhibit the proliferation of human chondrocytes through osteopontin (OPN). In the present study, we used online tools to figure out several candidates lncRNAs which were potentially correlated with miR-127-5p. Through assessing the expression levels of the candidates lncRNAs, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was chosen as a further research subject. MALAT1 knockdown significantly repressed human OA chondrocyte proliferation, as well as the protein levels of OPN, p-PI3K, and p-Akt in OA chondrocytes. As verified by luciferase assays, MALAT1 directly bound to miR-127-5p to inhibit miR-127-5p expression. Then we achieved miR-127-5p inhibition through miR-127-5p inhibitor transfection; the miR-127-5p inhibition could promote chondrocyte proliferation, as well as the protein levels of OPN, p-PI3K, and p-Akt; in addition, the MALAT1 knockdown partially reversed the promotive effect of miR-127-5p inhibition on chondrocyte proliferation, OPN and PI3K/Akt signaling-related protein levels. Taken together, MALAT1 could directly bind to miR-127-5p to inhibit its expression, so as to rescue OPN expression and promote chondrocyte proliferation through PI3K/Akt pathway. Targeting MALAT1 so as to rescue miR-127-5p expression in OA might help to inhibit chondrocyte proliferation through miR-127-5p-mediated OPN regulation and downstream PI3K/Akt pathway. J. Cell. Biochem. 119: 431-439, 2018. © 2017 Wiley Periodicals, Inc.
Asunto(s)
Proliferación Celular , Condrocitos/metabolismo , MicroARNs/metabolismo , Osteopontina/biosíntesis , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , ARN Largo no Codificante/metabolismo , Transducción de Señal , Células Cultivadas , Condrocitos/citología , HumanosRESUMEN
CONTEXT: Osteoarthritis (OA) is a common chronic degenerative joint disease resulting in physical disability and reduced quality of life. Different biochemical signaling pathways are involved in the progression of OA, including the c-Jun NH2-terminal kinase (JNK) signal transduction pathway. OBJECTIVE: In this study, we have reviewed the recent updates on the association of JNK pathway with OA. METHODS: In this review, we have explored the databases like PubMed, Google Scholar, Medline, Scopus, etc., and collected the most relevant papers of JNK signaling pathway involved in the pathogenesis and therapeutics of OA Results: JNK has been shown by scientific studies to be activated (phosphorylated) in OA that can play a key role in the cartilage destruction. Activation of JNK causes the phosphorylation of c-Jun that causes decreased proteoglycan synthesis and enhanced production of matrix metalloproteinase 13 (MMP-13). Overproduction of MMP-13 by chondrocytes plays a central role in cartilage degeneration in OA. Thus, targeting JNK pathway might be a promising therapeutic application for the prevention and treatment of OA. A number of JNK-inhibitors have been used in vitro and in vivo studies; however, not yet been translated into human use. CONCLUSIONS: This review study indicates that JNK pathway plays an important role in development and progression of OA, and targeting the JNK pathway might be a potential approach for the treatment of OA in future.