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Open Biol. 2014 Oct;4(10). pii: 140125. doi: 10.1098/rsob.140125.

Hsp10 nuclear localization and changes in lung cells response to cigarette smoke suggest novel roles for this chaperonin.

Author information

1
Istituto Euro-Mediterraneo di Scienza e Tecnologia (IEMEST), Palermo, Italy Dipartimento di Biomedicina Sperimentale e Neuroscienze Cliniche, Università degli Studi di Palermo, Palermo, Italy.
2
Dipartimento di Biomedicina Sperimentale e Neuroscienze Cliniche, Università degli Studi di Palermo, Palermo, Italy.
3
Laboratorio di Citoimmunopatologia dell'apparato cardio-respiratorio, Fondazione 'S. Maugeri' IRCCS, Istituto di Veruno, Veruno (NO), Italy.
4
HSR Giglio, Cefalù (PA), Italy.
5
Divisione di Pneumologia, Fondazione 'S. Maugeri' IRCCS, Istituto di Veruno, Veruno (NO), Italy.
6
Fondazione 'S. Maugeri' IRCCS, Istituto Scientifico di Cassano delle Murge, Cassano delle Murge (BA), Italy.
7
Dipartimento STEBICEF, Istituto Telethon Dulbecco c/o Universita' degli Studi di Palermo, Sezione di Biologia Cellulare, Palermo, Italy.
8
Department of Biology and Ecology "La Tuscia" University, Viterbo, Italy.
9
Department of Microbiology and Immunology, School of Medicine, University of Maryland at Baltimore, Baltimore, MD, USA IMET, Columbus Center, Baltimore, MD, USA.
10
Istituto Euro-Mediterraneo di Scienza e Tecnologia (IEMEST), Palermo, Italy Department of Microbiology and Immunology, School of Medicine, University of Maryland at Baltimore, Baltimore, MD, USA IMET, Columbus Center, Baltimore, MD, USA.
11
Istituto Euro-Mediterraneo di Scienza e Tecnologia (IEMEST), Palermo, Italy Dipartimento di Biomedicina Sperimentale e Neuroscienze Cliniche, Università degli Studi di Palermo, Palermo, Italy giampylr@hotmail.com giampiero.larocca@unipa.it.

Abstract

Heat-shock protein (Hsp)10 is the co-chaperone for Hsp60 inside mitochondria, but it also resides outside the organelle. Variations in its levels and intracellular distribution have been documented in pathological conditions, e.g. cancer and chronic obstructive pulmonary disease (COPD). Here, we show that Hsp10 in COPD undergoes changes at the molecular and subcellular levels in bronchial cells from human specimens and derived cell lines, intact or subjected to stress induced by cigarette smoke extract (CSE). Noteworthy findings are: (i) Hsp10 occurred in nuclei of epithelial and lamina propria cells of bronchial mucosa from non-smokers and smokers; (ii) human bronchial epithelial (16HBE) and lung fibroblast (HFL-1) cells, in vitro, showed Hsp10 in the nucleus, before and after CSE exposure; (iii) CSE stimulation did not increase the levels of Hsp10 but did elicit qualitative changes as indicated by molecular weight and isoelectric point shifts; and (iv) Hsp10 nuclear levels increased after CSE stimulation in HFL-1, indicating cytosol to nucleus migration, and although Hsp10 did not bind DNA, it bound a DNA-associated protein.

KEYWORDS:

COPD; Hsp10; bronchial epithelial cells; lung fibroblasts; nuclear localization

PMID:
25355063
PMCID:
PMC4221893
DOI:
10.1098/rsob.140125
[Indexed for MEDLINE]
Free PMC Article

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