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与脂多糖诱导的SW982细胞系炎症相关的透明质酸合酶基因表达的体外模型

In vitro model of hyaluronan synthase gene expression associated with lipopolysaccharide-induced inflammation in SW982 cell line.

作者信息

Viriyakhasem Nawarat, Khuajan Siriprapa, Kongtawelert Prachya, Panthong Ampai, Ongchai Siriwan, Reutrakul Vichai

机构信息

Thailand Excellence Center for Tissue Engineering and Stem Cells, Department of Biochemistry and the Center of Excellence for Innovation in Chemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.

出版信息

In Vitro Cell Dev Biol Anim. 2014 Oct;50(9):787-91. doi: 10.1007/s11626-014-9777-7. Epub 2014 Jun 17.

Abstract

The present study aimed to demonstrate the phenomena of hyaluronan synthesis in response to lipopolysaccharide-induced inflammation in SW982, a human synovial sarcoma cell line. The expression of IL-1ß, including Toll-like receptor 4 and IL-1ß-converting enzyme, was proved to be induced by a reverse transcription-polymerase chain reaction. The expression of HAS genes encoding enzyme hyaluronan synthase 2 and 3, including CD44 gene which encodes the cell surface receptor of hyaluronan were upregulated in association with the activation of inflammation, along with an increase in hyaluronan level in the culture medium. The highest expression of HAS2 and HAS3 was found at 9 h after treatment with lipopolysaccharide. However, HAS1 gene expression was not detectable neither with the non-treatment nor with the treatment with lipopolysaccharide. Dexamethasone at 30 nM significantly suppressed lipopolysaccharide-induced HAS genes expression, leading to the decline of the hyaluronan level in the culture medium. Our results demonstrated the effective tool for studying hyaluronan synthesis in association with inflammation in the SW982 cell line.

摘要

本研究旨在证明在人滑膜肉瘤细胞系SW982中,透明质酸合成对脂多糖诱导的炎症的反应现象。通过逆转录-聚合酶链反应证明,包括Toll样受体4和白细胞介素-1β转化酶在内的白细胞介素-1β的表达被诱导。编码透明质酸合酶2和3的HAS基因的表达,包括编码透明质酸细胞表面受体的CD44基因,随着炎症的激活而上调,同时培养基中透明质酸水平增加。脂多糖处理后9小时发现HAS2和HAS3的表达最高。然而,无论是未处理还是脂多糖处理,均未检测到HAS1基因表达。30 nM的地塞米松显著抑制脂多糖诱导的HAS基因表达,导致培养基中透明质酸水平下降。我们的结果证明了在SW982细胞系中研究与炎症相关的透明质酸合成的有效工具。

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