Proteasomes in lungs from organ donors and patients with end-stage pulmonary diseases

Title:

Proteasomes in lungs from organ donors and patients with end-stage pulmonary diseases

Creator:

Baker, T. A., Bach, H. H., Gamelli, R. L., Love, R. B., and Majetschak, M.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:7353d479-ab00-44a7-b751-13af35980df1
uuid:7353d479-ab00-44a7-b751-13af35980df1
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, plicní fibróza, pulmonary fibrosis, 20S proteasome, 26S proteasome, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, pulmonary sarcoidosis, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Proteasomes appear to be involved in the pathophysiology of various acute and chronic lung diseases. Information on the human lung proteasome in health and disease, however, is sparse. Therefore, we studied whether end-stage pulmonary diseases are associated with alterations in lung 20S/26S proteasome content, activity and 20S subunit composition. Biopsies were obtained from donor lungs (n=7) and explanted lungs from patients undergoing lung transplantation because of end stage chronic obstructive pulmonary disease (COPD; n=7), idiopathic pulmonary fibrosis (IPF, n=7) and pulmonary sarcoidosis (n=5). 20S/26S proteasomes in lung extracts were quantified by ELISA, chymotrypsin-like proteasome peptidase activities measured and 20S proteasome β subunits analyzed by Western blot. As compared with donor lungs, proteasome content was increased in IPF and sarcoidosis, but not in COPD. The relative distribution of free 20S and 26S proteasomes was similar; 20S proteasome was predominant in all extracts. Proteasome peptidase activities in donor and diseased lungs were indistinguishable. All extracts contained a mixed composition of inducible 20S β immuno-subunits and their constitutive counterparts; a disease associated distribution could not be identified. A higher content of lung proteasomes in IPF and pulmonary sarcoidosis may contribute to the pathophysiology of human fibrotic lung diseases., T. A. Baker, H. H. Bach IV, R. L. Gemelli, R. B. Love, M. Majetschak., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2014 Volume:63 | Number:3

Harvested from:

CDK

Metadata only:

false