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http://purl.uniprot.org/citations/24660549http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24660549http://www.w3.org/2000/01/rdf-schema#comment"

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."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.org/dc/terms/identifier"doi:10.7754/clin.lab.2013.130303"xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/author"Zimmermann M."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/author"Jung C."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/author"Yilmaz A."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/author"Figulla H.R."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/author"Ankersmit H.J."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/author"Lichtenauer M."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/author"Goebel B."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/author"Lauten A."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/author"Nickl S."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/author"Pistulli R."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/name"Clin Lab"xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/pages"323-328"xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/title"Transient hypoxia leads to increased serum levels of heat shock protein-27, -70 and caspase-cleaved cytokeratin 18."xsd:string
http://purl.uniprot.org/citations/24660549http://purl.uniprot.org/core/volume"60"xsd:string
http://purl.uniprot.org/citations/24660549http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24660549
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