Scarred lungs leave trail of beta arrestins

March 28, 2011, AAAS

Targeting a family of signaling proteins called beta arrestins may stop the life-threatening scarring and thickening of lungs associated with pulmonary fibrosis, reports a new Science study in mice.

If a drug that blocks the function of beta arrestins proves to be effective and safe in humans, patients and doctors will be able to add another treatment option to the currently sparse shelf of therapies. Under normal circumstances, the formation of is the result of the body’s own team of cellular doctors and nurses, rushing to help to seal up wounds with fibrous connective tissue and prevent infection.

But sometimes the formation of scar tissue can go haywire; progressive scarring and stiffening that occurs in the lungs of pulmonary fibrosis patients it increasingly difficult for affected individuals to breathe. The massive buildup of scar tissue can't be reversed, and no treatment has been able to stop progression of the disease. Most patients die within a few years of diagnosis. Discouragingly, no one knows what causes pulmonary fibrosis or even why some people get it while others don’t.

Because pulmonary fibrosis appears later in life and without warning, creating an animal model that directly mimics disease onset has been difficult. The standard way to study pulmonary fibrosis is to treat mice with an antibiotic that causes lung scarring similar to that found in the lungs of pulmonary fibrosis patients. Here, Paul Noble and colleagues show that deleting beta arrestin genes in mice protected the animals from developing antibiotic-induced fibrosis, without affecting normal wound healing.

The team also determined that beta arrestins regulate the ability of fibroblasts—cells that build collagen and connective tissue—to invade and damage lung tissue. By blocking beta arrestins’ ability to invade and degrade lung tissue, the researchers were able to halt the development of lung fibrosis in . Noble and colleagues also found that similarly, blocking the function of beta arrestins in fibroblast cells from pulmonary fibrosis patients reduced damage to tissue.

The results point to beta arrestins as a possible drug target for pulmonary fibrosis.

More information: "Beta-Arrestin Deficiency Protects Against Pulmonary Fibrosis in Mice and Prevents Fibroblast Invasion of Extracellular Matrix," by A.K. Lovgren Science (2011)

Related Stories

Recommended for you

Fabric imbued with optical fibers helps fight skin diseases

February 23, 2018
A team of researchers with Texinov Medical Textiles in France has announced that their PHOS-ISTOS system, called the Fluxmedicare, is on track to be made commercially available later this year. The system consists of a piece ...

DNA gets away: Scientists catch the rogue molecule that can trigger autoimmunity

February 22, 2018
A research team has discovered the process - and filmed the actual moment - that can change the body's response to a dying cell. Importantly, what they call the 'Great Escape' moment may one day prove to be the crucial trigger ...

Low-calorie diet enhances intestinal regeneration after injury

February 22, 2018
Dramatic calorie restriction, diets reduced by 40 percent of a normal calorie total, have long been known to extend health span, the duration of disease-free aging, in animal studies, and even to extend life span in most ...

Artificial intelligence quickly and accurately diagnoses eye diseases and pneumonia

February 22, 2018
Using artificial intelligence and machine learning techniques, researchers at Shiley Eye Institute at UC San Diego Health and University of California San Diego School of Medicine, with colleagues in China, Germany and Texas, ...

Gut microbes protect against sepsis—mouse study

February 22, 2018
Sepsis occurs when the body's response to the spread of bacteria or toxins to the bloodstream damages tissues and organs. The fight against sepsis could get a helping hand from a surprising source: gut bacteria. Researchers ...

Breakthrough could lead to better drugs to tackle diabetes and obesity

February 22, 2018
Breakthrough research at Monash University has shown how different areas of major diabetes and obesity drug targets can be 'activated', guiding future drug development and better treatment of diseases.

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.