Summary
Chronic obstructive pulmonary disease (COPD) is the fourth leading
cause of death in the United States. Current therapies for COPD only
address symptoms of the disease and are unable to correct the
underlying tissue defects associated with COPD that contribute to
airlow limitation, such as emphysema. One potential cause of
airflow limitation is due to a defect in the regulation of
prostaglandin E production, which is important in modulating
fibroblast repair functions within the lung. In COPD it is believed
that increased prostaglandin E production in the alveolar
fibroblasts inhibits repair functions leading to the development of
emphysema.

Researchers at the University of Nebraska have discovered a
microRNA capable of regulating the prostaglandin E pathway
which in turn modulates fibroblast repair function. This microRNA
was down regulated in alveolar fibroblasts obtained from COPD
patients. Reintroduction of this microRNA into the COPD fibroblasts
caused a significant decrease in prostaglandin E production. These
data provide a novel approach for effectively treating the COPD.

Market Value
The use of microRNA pathways to treat disease is an up and coming
field. COPD is a major health concern in the United States with very
limited therapeutic options. This technology provides a novel
method for treating one of the underlying causes of COPD.

Features and Benefits
• MicroRNAs show considerable specificity allowing therapies to
have fewer adverse effects than more generalized pathway
inhibitors
• The microRNA pathways can be targeted by microRNA like
agents or by approaches that modulate microRNA expression
• Has potential application in tissue repair outside of COPD

TID 199

Protection filed

UNeMed currently offers a variety of licensing options and collaborative development opportunities with the University of Nebraska Medical Center.