Upregulation of hepatic prolactin receptor gene expression by 17beta-estradiol following trauma-hemorrhage.
Upregulation of hepatic prolactin receptor gene expression by 17beta-estradiol following trauma-hemorrhage.
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创伤出血后 17β-雌二醇上调肝催乳素受体基因表达。
DOI：
10.1152/japplphysiol.00681.2003
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Chaudry,IrshadH
中科院分区：
文献类型：
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作者：
Yokoyama,Yukihiro;Kitchens,WilliamsC;Toth,Balazs;Schwacha,MartinG;Bland,KirbyI;Chaudry,IrshadH
虽然研究表明17β-雌二醇（E2）或催乳素（PRL）治疗对创伤-出血（TH）后的雄性大鼠具有保护作用，但这些药物的有益作用机制仍不清楚。由于E2调节肝脏中PRL受体（PRL-R）的表达，我们检测了T-H后E2处理是否对肝脏PLR-R基因表达有任何影响。雄性Sprague-Dawley大鼠经受创伤（即，5-cm中线剖腹术）和出血（35-40 mmHg持续90 min），随后进行液体复苏（乳酸林格氏液）或假手术，然后在复苏前立即用E2（50 μg/kg体重sc）或溶媒处理。3 h后收集肝脏样本，通过PCR测定PRL-R mRNA表达。肝脏PRL-R短型基因的表达不受T-H的影响，而长型基因的表达受到抑制。用E2处理T-H大鼠显著增加PRL-R短型基因表达，并使PRL-R长型基因表达恢复到假手术水平。在分离的肝细胞中，PRL-R短型基因表达与长型基因相比占主导地位。相反，在枯否细胞中仅检测到短型。E2体外处理显示肝细胞中PRL-R长型基因表达增加，但E2对枯否细胞或肝细胞中PRL-R短型基因表达无影响。因此，雄性T-H后E2处理似乎直接上调肝细胞中PRL-R长型基因的表达。然而，PRL-R短型的上调可能涉及肝脏中多种细胞类型的相互作用。
Although studies show protective effects of 17β-estradiol (E2) or prolactin (PRL) treatment in male rats after trauma-hemorrhage (TH), the mechanism of the salutary effects of these agents remains unknown. Because E2modulates PRL receptor (PRL-R) expression in the liver, we examined whether E2treatment after T-H has any effects on hepatic PLR-R gene expression. Male Sprague-Dawley rats were subjected to trauma (i.e., 5-cm midline laparotomy) and hemorrhage (35–40 mmHg for 90 min) followed by fluid resuscitation (Ringer lactate) or sham operation and then treated with E2(50 μg/kg body wt sc) or vehicle immediately before resuscitation. Liver samples were collected at 3 h thereafter, and PRL-R mRNA expression was determined by PCR. Liver expression of PRL-R short-form gene was unaffected by T-H, whereas that of the long-form gene was suppressed. Treatment of T-H rats with E2significantly increased PRL-R short-form gene expression and normalized PRL-R long-form gene expression to sham levels. In the isolated hepatocytes, PRL-R short-form gene expression was predominant compared with the long-form gene. In contrast, only the short form was detected in Kupffer cells. In vitro treatment by E2demonstrated an increase in the PRL-R long-form gene in hepatocytes, but E2had no effect on PRL-R short-form gene expression in either the Kupffer cells or hepatocytes. Thus E2treatment after T-H in males appears to directly upregulate PRL-R long-form gene expression in hepatocytes. However, the upregulation of the PRL-R short form might involve the interaction of multiple cell types in the liver.