h-89 has been researched along with Hemorrhage* in 2 studies
2 other study(ies) available for h-89 and Hemorrhage
| Article | Year |
|---|---|
G-protein-coupled receptor 30 mediates estrogen's nongenomic effects after hemorrhagic shock and trauma.
Topics: Animals; Cyclic AMP-Dependent Protein Kinases; Estradiol; Estrogen Receptor alpha; Estrogens, Conjugated (USP); Hemorrhage; Hepatocytes; Isoquinolines; Liver; Models, Biological; Protein Kinase Inhibitors; Rats; Receptors, G-Protein-Coupled; RNA, Small Interfering; Serum Albumin, Bovine; Signal Transduction; Sulfonamides; Transfection; Wounds and Injuries | 2007 |
G protein-coupled receptor 30-dependent protein kinase A pathway is critical in nongenomic effects of estrogen in attenuating liver injury after trauma-hemorrhage.
Although nongenomic effects of 17beta-estradiol (E2) are mediated via the estrogen receptor alpha (ER-alpha), the existence of another novel ER, G protein-coupled receptor 30 (GPR30), has been suggested as a candidate for triggering a broad range of E2-mediated signaling. GPR30 also acts independently of the ER to promote activation of the protein kinase A (PKA) pathway, which protects cells from apoptosis through Bcl-2. In this study, we examined whether the salutary effects of E2 in attenuating hepatic injury after trauma-hemorrhage are mediated via GPR30- or ER-alpha-regulated activation of PKA-dependent signaling. At 2 hours after trauma-hemorrhage, administration of E2-conjugated to bovine serum albumin (E2-BSA, membrane impermeable) or E2 induced the up-regulation of ER-alpha and GPR30 and attenuated hepatic injury. This was accompanied by increases in PKA activity and Bcl-2 expression. Inhibition of PKA in E2-BSA-treated trauma-hemorrhage rats by PKA inhibitor H89 prevented the E2-BSA attenuation of hepatic injury. Isolated hepatocytes were transfected with small interfering RNA to suppress GPR30 or ER. We found that suppression of GPR30 but not ER-alpha prevented E2-BSA- or E2-induced PKA activation and Bcl-2 expression. These results suggest that the nongenomic salutary effect of E2 in reducing hepatic injury after trauma-hemorrhage is mediated through the PKA-dependent pathway via GPR30 but not ER-alpha. Topics: Animals; Blotting, Western; Cyclic AMP-Dependent Protein Kinases; Estradiol; Estrogen Receptor alpha; Estrogens, Conjugated (USP); Glutathione Transferase; Hemorrhage; Hepatocytes; Isoenzymes; Isoquinolines; Liver; Male; Models, Biological; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-bcl-2; Rats; Rats, Sprague-Dawley; Receptors, G-Protein-Coupled; RNA, Small Interfering; Serum Albumin, Bovine; Signal Transduction; Sulfonamides; Transfection; Wounds and Injuries | 2007 |