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Biochem Biophys Res Commun. 2014 Mar 7;445(2):369-74. doi: 10.1016/j.bbrc.2014.02.009. Epub 2014 Feb 10.

Deficiency of developmental endothelial locus-1 (Del-1) aggravates bleomycin-induced pulmonary fibrosis in mice.

Author information

1
Department of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea; Department of Pharmacology, University of Ulsan College of Medicine, Seoul, Republic of Korea.
2
Department of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea; Department of Pharmacology, University of Ulsan College of Medicine, Seoul, Republic of Korea. Electronic address: choieun@ulsan.ac.kr.

Abstract

Pulmonary fibrosis is a lung disease wherein lung parenchyma is gradually and irreversibly replaced with collagen. The molecular pathogenesis of pulmonary fibrosis is not fully understood and the only effective treatment available is lung transplantation. To test if Del-1, an endogenous anti-inflammatory molecule, may be implicated in the development of pulmonary fibrosis, we induced pulmonary fibrosis in wild type (WT) and Del-1(-/-) mice by intratracheal administration of bleomycin. Del-1 expression in the lung was decreased in the WT mice treated with bleomycin compared to control mice. In addition, bleomycin-induced pulmonary fibrosis increased collagen deposition and TGF-β production in the lung of Del-1(-/-) mice. Finally, Del-1(-/-) mice treated with bleomycin displayed higher weight loss and greater mortality than did WT mice identically treated. These findings suggest that Del-1 may negatively regulate development of pulmonary fibrosis. Further delineation of a role for Del-1 in the development of pulmonary fibrosis will broaden our understanding of the molecular pathogenesis of this disease and hopefully help develop potential therapeutics.

KEYWORDS:

Collagen; Del-1 (developmental endothelial locus-1); Inflammation; Pulmonary fibrosis; Transforming growth factor-beta

PMID:
24525119
DOI:
10.1016/j.bbrc.2014.02.009
[Indexed for MEDLINE]

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