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Articles in PresS, published online ahead of print January 3, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00682.2001
Submitted on July 31, 2001
Accepted on December 24, 2001
1 Department of Pathology, Duke University, Durham, NC, USA; Cell and Molecular Biology Program, Duke University, Durham, NC, USA
2 Department of Radiation Oncology, Duke University, Durham, NC, USA
3 Department of Pathology, Duke University, Durham, NC, USA
4 Department of Radiation Oncology, Duke University, Durham, NC, USA; Department of Pathology, Duke University, Durham, NC, USA
* To whom correspondence should be addressed. E-mail: laura.hale{at}duke.edu.
Our previous studies using oxygen microelectrodes showed that the thymus is grossly hypoxic under normal physiologic conditions. We now investigate how oxygen tension affects the thymus at the cell and molecular level. Adducts of the pimonidazole hypoxia marker drug accumulate in foci within the cortex and medulla and at the corticomedullary junction, consistent with the presence of widespread cellular hypoxia in normal thymus. Hypoxia-associated pimonidazole accumulation was decreased but not abrogated by oxygen administration. Genes previously reported to be induced by hypoxia are expressed at baseline levels in normal thymus, indicating that physiologic adaptation to hypoxia has occurred. Despite changes in thymus size and cellularity, thymic pO2 does not change with age. Combined assays for hypoxia and cell death show that hypoxia achieved either using hypoxic gas mixtures or high-density culture in normoxia decreases spontaneous thymocyte apoptosis in vitro. Taken together, these data suggest that regulatory mechanisms exist to maintain thymic cellular hypoxia in vivo and that oxygen tension may regulate thymocyte survival both in vitro and in vivo.
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