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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Sessa, William C. Feng, Yan Velazquez, Heino Goodwin, Julie E. |
| Description | Author Affiliation: Goodwin JE ( Department of Pediatrics,Yale University School of Medicine, New Haven, CT 06520, USA. julie.goodwin@yale.edu); |
| Abstract | The glucocorticoid receptor (GR) is ubiquitously expressed on nearly all cell types, but tissue-specific deletion of this receptor can produce dramatic whole organism phenotypes. In this study we investigated the role of the endothelial GR in sepsis in vivo and in vitro. Mice with an endothelial-specific GR deletion and controls were treated with 12.5 mg/kg LPS and phenotyped. Mice lacking GR showed significantly increased mortality, more hemodynamic instability, higher nitric oxide levels, and higher levels of the inflammatory cytokines, tumor necrosis factor-alpha (TNF- ) and interleukin-6 (IL-6) compared with controls. There were no differences in rates of apoptosis or macrophage recruitment between the two groups. Both endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) expression were increased after LPS challenge in mice with endothelial GR deficiency, and aminoguanidine, a specific iNOS inhibitor in mice was able to rescue hemodynamic collapse in these animals. In vitro, human umbilical vein cells (HUVECs) subjected to GR knockdown by siRNA showed increased expression of eNOS at baseline that persisted after treatment with LPS. Both eNOS and iNOS mRNA was increased by qPCR. In HUVECs lacking GR, NF-κB levels and NF-κB-dependent genes tissue factor and IL-6 were increased compared with controls. Thus, endothelial GR is a critical regulator of NF-κB activation and nitric oxide synthesis in sepsis. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 1 |
| Volume Number | 110 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2013-01-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Endothelium Metabolism NF-kappa B Receptors, Glucocorticoid Sepsis Animals Apoptosis Physiology Corticosterone Blood Gene Deletion Hemodynamics Human Umbilical Vein Endothelial Cells In Situ Nick-End Labeling Interleukin-6 Lipopolysaccharides Administration & Dosage Toxicity Mice Mice, Knockout Nitric Oxide Nitric Oxide Synthase Type II Nitric Oxide Synthase Type III Genetics Prevention & Control Tumor Necrosis Factor-alpha Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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