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肾上腺间隙连接蛋白表达的调节。

Modulation of adrenal gap junction expression.

作者信息

Murray S A, Shah U S

机构信息

Department of Cell Biology and Physiology, University of Pittsburgh, School of Medicine, Pennsylvania 15261, USA.

出版信息

Horm Metab Res. 1998 Jun-Jul;30(6-7):426-31. doi: 10.1055/s-2007-978909.

Abstract

To increase our knowledge of the role of peptide hormone stimulation in gap junction protein expression and adrenal cortical cell function, primary rat adrenal cortical cells were treated with adrenocorticotropin, and gap junction proteins were measured. Immunocytochemistry and western blot analysis were used to detect and characterize gap junction type and distribution. The gap junction protein, connexin 43 (alpha 1), was detected. Analysis of six connexin protein types did not reveal gap junction species other than alpha 1. Cells of the inner adrenal cortical zones, zonae fasciculata and reticularis, were demonstrated to have the highest number of gap junctions per cell in the adrenal gland. Adrenal cell cultures enriched for the two inner cortical adrenal zones were established and demonstrated also to express alpha 1 gap junction protein. Adrenocorticotropin (40 mUnits/ml) and dibutyryl cyclic adenosine monophosphate (1 mM) treatments increased alpha 1 gap junction protein levels and decreased cell proliferation rates in the cell cultures. The results are consistent with the hypothesis that gap junction expression can be regulated by adrenocorticotropin acting through the second messenger cyclic adenosine monophosphate. It can be suggested that gap junction expression in the adrenal gland may be under hormonal influence, and that gap junctions serve as passage for movement of molecules involved in control of cell proliferation.

摘要

为了增加我们对肽类激素刺激在缝隙连接蛋白表达和肾上腺皮质细胞功能中作用的了解,我们用促肾上腺皮质激素处理原代大鼠肾上腺皮质细胞,并检测缝隙连接蛋白。采用免疫细胞化学和蛋白质印迹分析来检测和鉴定缝隙连接的类型及分布。检测到了缝隙连接蛋白连接蛋白43(α1)。对六种连接蛋白类型的分析未发现除α1以外的缝隙连接种类。肾上腺皮质内带束状带和网状带的细胞被证明是肾上腺中每个细胞缝隙连接数量最多的。建立了富含肾上腺皮质内两个带的肾上腺细胞培养物,并证明其也表达α1缝隙连接蛋白。促肾上腺皮质激素(40毫单位/毫升)和二丁酰环磷酸腺苷(1毫摩尔)处理可提高细胞培养物中α1缝隙连接蛋白水平,并降低细胞增殖率。这些结果与以下假设一致,即缝隙连接表达可由通过第二信使环磷酸腺苷起作用的促肾上腺皮质激素调节。可以推测,肾上腺中的缝隙连接表达可能受激素影响,并且缝隙连接充当参与细胞增殖控制的分子移动的通道。

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