Format

Send to

Choose Destination
Biochem Biophys Res Commun. 2013 Sep 20;439(2):315-20. doi: 10.1016/j.bbrc.2013.07.012. Epub 2013 Jul 15.

Romo1 expression contributes to oxidative stress-induced death of lung epithelial cells.

Author information

1
Department of Internal Medicine, Yonsei University College of Medicine, Yonsei University Health System, Seoul 135-270, Republic of Korea.

Abstract

Oxidant-mediated death of lung epithelial cells due to cigarette smoking plays an important role in pathogenesis in lung diseases such as idiopathic pulmonary fibrosis (IPF). However, the exact mechanism by which oxidants induce epithelial cell death is not fully understood. Reactive oxygen species (ROS) modulator 1 (Romo1) is localized in the mitochondria and mediates mitochondrial ROS production through complex III of the mitochondrial electron transport chain. Here, we show that Romo1 mediates mitochondrial ROS production and apoptosis induced by oxidative stress in lung epithelial cells. Hydrogen peroxide (H2O2) treatment increased Romo1 expression, and Romo1 knockdown suppressed the cellular ROS levels and cell death triggered by H2O2 treatment. In immunohistochemical staining of lung tissues from patients with IPF, Romo1 was mainly localized in hyperplastic alveolar and bronchial epithelial cells. Romo1 overexpression was detected in 14 of 18 patients with IPF. TUNEL-positive alveolar epithelial cells were also detected in most patients with IPF but not in normal controls. These findings suggest that Romo1 mediates apoptosis induced by oxidative stress in lung epithelial cells.

KEYWORDS:

Idiopathic pulmonary fibrosis; Lung injury; Oxidative stress; Reactive oxygen species; Romo1

PMID:
23867822
DOI:
10.1016/j.bbrc.2013.07.012
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center