Fixing Iron Levels In Lung Cells Could Treat COPD
Drug Development: Study shows that concentrations of the metal inside cell organelles increase in mice with the disease
By Michael Torrice
Chemical & Engineering News
ISSN 0009-2347
Volume 94 Issue 3 | News of The Week
Issue Date: January 18, 2016 | Web Date: January 13, 2016

Patients with chronic obstructive pulmonary disease (COPD)--a group of disorders that include chronic bronchitis and emphysema--struggle to breathe and rely on drugs called bronchodilators to widen their obstructed airways. But these drugs just relieve
symptoms of COPD and don't stop the underlying mechanisms that cause this progressive disease.
A new study suggests a possible COPD mechanism, offering a novel therapeutic strategy for the disease, which is one of the top five causes of death worldwide.
The scientists report that iron levels in the mitochondria of lung cells are elevated in COPD, damaging the critical cellular powerhouses. A small molecule capable of sequestering iron restored proper levels of the metal, preventing, and even reversing,
lung inflammation and injury in a mouse model of COPD (Nat. Med. 2016, DOI: 10.1038/nm.4021).
Smoking is the number one risk factor for COPD. But only a fraction of smokers get the disease. This has led researchers to look for genetic factors that make people susceptible to developing it. One such gene codes for iron-responsive element-binding
protein 2 (IRP2). Levels of IRP2 are elevated in the lungs of COPD patients. Augustine M. K. Choi of Weill Cornell Medical College and his colleagues wanted to understand how this protein is involved in the disease.
The team studied mice that had spent two hours per day for up to six months in a chamber filled with cigarette smoke. Normal mice developed a COPD-like disease, but mice genetically engineered to lack the IRP2 gene did not.
An analysis of genes regulated by IRP2 suggested that the protein's main effects were in cells' mitochondria. When the researchers studied the mitochondria of COPD mice, they found that the organelles were dysfunctional and damaged. In particular they
had elevated levels of one form of cellular iron.
Normal mice that were given deferiprone, an FDA-approved iron-chelating drug, and then exposed to cigarette smoke didn't develop the COPD-like disease. In animals that had already developed the disease, the drug improved symptoms and lowered
mitochondrial iron levels.
Peter J. Barnes, head of respiratory medicine at Imperial College London, says the researchers next need to show that this mechanism is relevant in people. "Mice can be misleading in the context of COPD," he says. "All mice exposed to cigarette smoke get
COPD, while not all humans do." Barnes suggests investigating whether mitochondrial iron levels are disrupted in COPD patients.


Copyright (c) 2016 American Chemical Society

Department: Science & Technology
News Channels: Biological SCENE
Keywords: chronic obstructive pulmonary disease, COPD, lungs, iron, chelation

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