Targeting matrix metalloproteinase-13 in bronchial epithelial repair

Christopher Howell, James R. Smith, Janis K. Shute
  • Clinical & Experimental Allergy, July 2018, Wiley
  • DOI: 10.1111/cea.13215

Enhancing lung airway repair: implications for asthma and COPD

Photo by Chris Keats on Unsplash

Photo by Chris Keats on Unsplash

What is it about?

The paper describes the action of a virus model (polyI:C) on the lining of lung cells (bronchial epithelial cells) followed using time-lapse microscopy. MMP‐13 (an enzyme involved in collagen restructuring) and endothelin (a vasoconstricting peptide involved in lung and other diseases) were also released. Inhibitors of MMP‐13 activity (WAY 170523) and expression (dimethyl fumarate) significantly enhanced the rate of repair. Bosentan (an endothelin receptor drug) enhanced the rate of bronchial epithelial repair by a mechanism that was independent of MMP‐13.

Why is it important?

Bronchial epithelial repair is limited by endothelin and by MMP‐13, a protease that degrades coagulation factors, such as fibrinogen, and matrix proteins essential for epithelial repair. Further studies with primary cells from patients are needed to confirm whether repurposing bosentan and inhibitors of MMP‐13 expression or activity, for inhalation may be useful therapeutic strategies in diseases where repeated cycles of epithelial injury and repair occur, such as in asthma and COPD.

Perspectives

Dr James R Smith
University of Portsmouth

A free post-print version of the paper is available for download from the resources section (right-hand-side panel).

Read Publication

http://dx.doi.org/10.1111/cea.13215

The following have contributed to this page: Dr James R Smith