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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Marsden, Philip A. Dattani, Neil D. Heximer, Scott P. Ho, J. J. David Adamson, S. Lee Lidington, Darcy Connelly, Kim A. Mazer, C. David Chen, Kevin M. El-beheiry, Mostafa H. Wilson, David F. Bolz, Steffen-sebastian Henkelman, R. Mark Tsui, Albert K. Y. Hare, Gregory M. T. |
| Description | Author Affiliation: Tsui AK ( Department of Anesthesia, St. Michael's Hospital, University of Toronto, Keenan Research Centre in the Li Ka Shing Knowledge Institute, Toronto, ON, Canada M5B 1W8.); |
| Abstract | Cells sense and respond to changes in oxygen concentration through gene regulatory processes that are fundamental to survival. Surprisingly, little is known about how anemia affects hypoxia signaling. Because nitric oxide synthases (NOSs) figure prominently in the cellular responses to acute hypoxia, we defined the effects of NOS deficiency in acute anemia. In contrast to endothelial NOS or inducible NOS deficiency, neuronal NOS (nNOS)(-/-) mice demonstrated increased mortality during anemia. Unlike wild-type (WT) animals, anemia did not increase cardiac output (CO) or reduce systemic vascular resistance (SVR) in nNOS(-/-) mice. At the cellular level, anemia increased expression of HIF-1 protein and HIF-responsive mRNA levels (EPO, VEGF, GLUT1, PDK1) in the brain of WT, but not nNOS(-/-) mice, despite comparable reductions in tissue PO(2). Paradoxically, nNOS(-/-) mice survived longer during hypoxia, retained the ability to regulate CO and SVR, and increased brain HIF- protein levels and HIF-responsive mRNA transcripts. Real-time imaging of transgenic animals expressing a reporter HIF- (ODD)-luciferase chimeric protein confirmed that nNOS was essential for anemia-mediated increases in HIF- protein stability in vivo. S-nitrosylation effects the functional interaction between HIF and pVHL. We found that anemia led to nNOS-dependent S-nitrosylation of pVHL in vivo and, of interest, led to decreased expression of GSNO reductase. These findings identify nNOS effects on the HIF/pVHL signaling pathway as critically important in the physiological responses to anemia in vivo and provide essential mechanistic insight into the differences between anemia and hypoxia. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 42 |
| Volume Number | 108 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2011-10-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Anemia Physiopathology Hypoxia-Inducible Factor 1, Alpha Subunit Metabolism Nitric Oxide Synthase Type I Adaptation, Physiological Genetics Animals Brain Blood Supply Cardiac Output Human Umbilical Vein Endothelial Cells Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Deficiency Oxygen Blood RNA, Messenger Signal Transduction Vascular Resistance Von Hippel-Lindau Tumor Suppressor Protein Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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