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维甲酸在转录后水平增强大鼠肝上皮细胞中连接蛋白43的表达。

Retinoic acid enhances connexin43 expression at the post-transcriptional level in rat liver epithelial cells.

作者信息

Bex V, Mercier T, Chaumontet C, Gaillard-Sanchez I, Flechon B, Mazet F, Traub O, Martel P

机构信息

Institut National de la Recherche Agronomique, Laboratoire de Nutrition et Sécurité Alimentaire, Jouy-en-Josas, France.

出版信息

Cell Biochem Funct. 1995 Mar;13(1):69-77. doi: 10.1002/cbf.290130112.

Abstract

The mechanism by which all-trans retinoic acid (RA) stimulates gap junctional intercellular communication (GJIC) in the rat liver epithelial cell line. IAR203, was investigated. When RA, at 0.1 microM for 24-48 h, enhanced the dye transfer in IAR203 cells (x 1.4), it increased the amount of connexin43 (Cx43) in the cell-cell contact regions of the plasma membrane, as evidenced by analysis by Western blot and by immunofluorescence. It had no effect on the level of Cx43 mRNA. Freeze-fracture analysis of the size of gap junctions revealed an increase of the proportion of small gap junctions in RA-treated cells. We conclude that, in IAR203 cells, RA stimulates GJIC by acting at the post-transcriptional level of Cx43 regulation. The possibility that RA acts indirectly on the regulation of Cx43 expression, and increases the half-life of Cx43 by inducing adhesion molecules is discussed.

摘要

研究了全反式维甲酸(RA)刺激大鼠肝上皮细胞系IAR203中缝隙连接细胞间通讯(GJIC)的机制。当RA以0.1微摩尔浓度作用24至48小时时,IAR203细胞中的染料转移增强(增加了1.4倍),同时通过蛋白质免疫印迹分析和免疫荧光证明,质膜细胞 - 细胞接触区域中连接蛋白43(Cx43)的量增加。RA对Cx43 mRNA水平没有影响。对缝隙连接大小的冷冻蚀刻分析显示,经RA处理的细胞中小缝隙连接的比例增加。我们得出结论,在IAR203细胞中,RA通过作用于Cx43调节的转录后水平来刺激GJIC。还讨论了RA间接作用于Cx43表达调节并通过诱导粘附分子增加Cx43半衰期的可能性。

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