Hepatic gene expression patterns following trauma-hemorrhage: effect of posttreatment with estrogen. 
The aim of this study was to examine the role of estrogen on hepatic gene expression profiles at an early time point following trauma-hemorrhage in rats.  Groups of injured and sham controls receiving estrogen or vehicle were killed 2 h after injury and resuscitation, and liver tissue was harvested.  Complementary RNA was synthesized from each RNA sample and hybridized to microarrays.  A large number of genes were differentially expressed at the 2-h time point in injured animals with or without estrogen treatment.  The upregulation or downregulation of a cohort of 14 of these genes was validated by reverse transcription-polymerase chain reaction.  This large-scale microarray analysis shows that at the 2-h time point, there is marked alteration in hepatic gene expression following trauma-hemorrhage.  However, estrogen treatment attenuated these changes in injured animals.  Pathway analysis demonstrated predominant changes in the expression of genes involved in metabolism, immunity, and apoptosis.  Upregulation of low-density lipoprotein receptor, protein phosphatase 1, regulatory subunit 3C, ring-finger protein 11, pyroglutamyl-peptidase I, bactericidal/permeability-increasing protein, integrin, αD, BCL2-like 11, leukemia inhibitory factor receptor, ATPase, Cu transporting, α polypeptide, and Mk1 protein was found in estrogen-treated trauma-hemorrhaged animals.  Thus, estrogen produces hepatoprotection following trauma-hemorrhage likely via antiapoptosis and improving/restoring metabolism and immunity pathways.