Abstract
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Transient Hypoxia Leads to Increased Serum Levels of Heat Shock Protein-27, -70 and Caspase-Cleaved Cytokeratin 18
by Michael Lichtenauer, Matthias Zimmermann, Stefanie Nickl, Alexander Lauten, Bjoern Goebel, Rudin Pistulli, Atilla Yilmaz, Hans-reiner Figulla, Hendrik Jan Ankersmit, Christian Jung
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Background: Chronic obstructive pulmonary disease (COPD) is a worldwide burden. We have previously shown that elevated levels of heat shock protein-27 (HSP27), -70 (HSP70), and caspase-cleaved cytokeratin 18 (ccCK-18) were found in serum of COPD patients correlating with disease severity. We hypothesized that transient hypoxia triggers the release of HSPs and ccCK-18.
Methods: Fourteen healthy volunteers were subjected to transient normobaric hypoxia in an air-conditioned hypoxia chamber simulating an oxygen concentration at an altitude of up to 5500 meters. Serum samples were evaluated for HSP27, -70, and ccCK-18.
Results: Baseline concentrations were 2760 pg/mL ± 517 SEM for HSP-27, 49 pg/mL ± 22 SEM for HSP-70, and 226 U/L ± 20 SEM for ccCK-18. After eight hours and an altitude equivalent of 5500 meters a significant increase was recorded, depicted by serum levels of 3737 pg/mL ± 571 SEM for HSP-27, 202 pg/mL ± 81 SEM for HSP-70, and 244 U/L ± 20 SEM for ccCK-18 (p < 0.05).
Conclusions: These results provide an explanation for the elevated serum levels of HSP-27, HSP-70, and ccCK-18 found in COPD patients, indicating that hypoxic conditions can trigger the release of the aforementioned factors.
DOI: 10.7754/Clin.Lab.2013.130303
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