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首页> 外文期刊>Journal of Cellular Physiology >Posttranscriptional regulation of connexin 32 expression in liver during acute inflammation.
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Posttranscriptional regulation of connexin 32 expression in liver during acute inflammation.

机译：转录后的调控联接蛋白32表达在肝脏急性炎症。

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摘要

Gap junctions mediate the communication between adjacent cells in tissues. In the liver, connexin 32 (Cx32) subunits make up the predominating gap junctions. The expression of Cx32 gene has been observed to be down-regulated in response to inflammatory states and during liver regeneration. In the present study we attempt to elucidate the molecular mechanisms underlying the down-regulation of the Cx32 expression during acute inflammation. A decrease in the level of Cx32 mRNA in rat liver occurred between 3 and 6 h after intravenous administration of bacterial lipopolysaccharide (LPS), simultaneously with the induction of an acute inflammatory response characterized by an increase in the level for beta-fibrinogen and a reduction of phosphoenolpyruvate carboxykinase mRNA. The reduction in Cx32 steady-state mRNA levels appears to occur at the posttranscriptional level, since the rate of degradation of this message seems to be higher than the rate of transcription of the gene. Degradation of Cx32 mRNA was blocked by the administration of actinomycin D, but not by cycloheximide, prior to injection of LPS. The stabilization of Cx32 message by actinomycin D correlated with the preservation of Cx32 on the cell surface, which otherwise disappears after administration of LPS alone. These results suggest that cellular communication via gap junctions could be regulated at the level of gene expression, by a posttranscriptional mechanism, during acute inflammatory states.
机译：缝隙连接调解之间的通信相邻的细胞组织。32 (Cx32)亚基组成主差距连接。观察到抑制在回应在肝脏炎症状态和再生。阐明背后的分子机制下调的Cx32表达式中急性炎症。Cx32 mRNA在大鼠肝脏发生3至6小时静脉注射后政府的细菌脂多糖(LPS),同时用诱导的急性炎症反应特点是水平的增加beta-fibrinogen和减少磷酸烯醇丙酮酸carboxykinase mRNA。减少Cx32稳态mRNA水平似乎发生在转录后的水平,自降解率消息似乎比率高基因的转录。信使rna被管理的放线菌素D,但不是由环己酰亚胺,之前注入的有限合伙人。放线菌素D的相关消息保护Cx32在细胞表面,否则管理有限合伙人后消失一个人。通过缝隙连接通讯调控基因表达水平的,转录后的机制,在急性炎症状态。

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