Hemoglobin alpha and beta are ubiquitous in the human lung, decline in idiopathic pulmonary fibrosis but not in COPD

Ishikawa Nobuhisa

Ohlmeier Steffen

Salmenkivi Kaisa

Myllarniemi Marjukka

Rahman Irfan

Mazur Witold

Kinnula Vuokko L.

Respiratory Research

Background: Idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD) are disorders of the lung parenchyma. They share the common denominators of a progressive nature and poor prognosis. The goal was to use non-biased proteomics to discover new markers for these diseases. Methods: Proteomics of fibrotic vs. control lung tissue suggested decreased levels of several spots in the lung specimens of IPF patients, which were identified as Hemoglobin (Hb) alpha and beta monomers and Hb alpha complexes. The Hb alpha and beta monomers and complexes were investigated in more detail in normal lung and lung specimens of patients with IPF and COPD by immunohistochemistry, morphometry and mass spectrometry (MS). Results: Both Hb monomers, in normal lung, were expressed especially in the alveolar epithelium. Levels of Hb alpha and beta monomers and complexes were reduced/lost in IPF but not in the COPD lungs when compared to control lung. MS-analyses revealed Hb alpha modification at cysteine105 (Cys alpha 105), preventing formation of the Hb alpha complexes in the IPF lungs. Hb alpha and Hb beta were expressed as complexes and monomers in the lung tissues, but were secreted into the bronchoalveolar lavage fluid and/or induced sputum supernatants as complexes corresponding to the molecular weight of the Hb tetramer. Conclusions: The abundant expression of the oxygen carrier molecule Hb in the normal lung epithelium and its decline in IPF lung are new findings. The loss of Hb complex formation in IPF warrants further studies and may be considered as a disease-specific modification.

医学 [ 490 ]

英語

BioMed Central Ltd

Copyright (c) 2010 Ishikawa et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

[ISSN] 1465-9921

[DOI] 10.1186/1465-9921-11-123

[NCID] AA12051434

[DOI] http://dx.doi.org/10.1186/1465-9921-11-123