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Articles in PresS, published online ahead of print October 29, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00058.2002
Submitted on February 11, 2002
Accepted on October 22, 2002
1 Department of Medicine, Brigham and Women's Hospital, Harvard Institutes of Medicine, Boston, MA, USA
2 Department of Pathology, University of Massachusetts Medical School, Worcester, MA, USA
3 Department of Surgery, University of California, San Francisco, San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: sgullans{at}rics.bwh.harvard.edu.
Renal medullary cells are exposed to elevated and variable osmolarities and low oxygen tension. Despite the harsh environment, these cells are resistant to the effects of many harmful events. To test the hypothesis that this resistance is a consequence of these cells developing a stress tolerance phenotype to survive in this milieu, we created osmotically tolerant cells (HT cells), by gradually adapting mIMCD3 cells to hyperosmotic medium containing NaCl and urea. HT cells have a reduced DNA synthesis rate, with the majority of cells arrested in the G0/G1 phase of the cell cycle and show constitutive expression of Hsp70 that is proportional to the degree of hyperosmolarity. Unlike acute, chronic hyperosmolarity failed to activate MAPKs. Moreover, HT cells acquired protein translational tolerance to further stress treatment, suggesting that HT cells have an osmotolerant phenotype, analogous to thermotolerance, but a permanent condition. Additionally to osmotic shock, HT cells were more resistant to heat, H2O2, cyclosporin, and apoptotic inducers, compared to isotonic mIMCD3 cells, but less resistant to amphotericin B and cadmium. HT cells demonstrate that in renal medullary cells, hyperosmotic stress activates biological processes that confer cross-tolerance to other stressful conditions.
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