Amy Firth, Ph.D.
University of Southern California
Funded by the American Lung Association of the Upper Midwest
Harnessing Power of a Protein to Improve Lung Repair Following Injury
The airways play an important role in lung defense, and have a remarkable capacity for repair upon injury. This repair process is abnormal in many lung diseases, including chronic obstructive pulmonary disease (COPD) . Using human cells and animal models of lung injury, we will study a protein called Claudin 18.1, which is found in cells lining the airways. We will look at how Claudin 18.1 influences function of airway stem cells, which are able to differentiate into specialized cell types to promote repair after injury. We hope to identify a novel approach to harness stem cell function by modulating Claudin 18 to improve lung repair following injury.
Update: So far we have observed that Claudin 18.1 is increasingly detected during the process in which stem cells differentiate into specialized cell types in cells lining the airways. We have made significant progress toward proving our central hypothesis that CLDN18.1-mediated signaling can stimulate pulmonary stem cell proliferation and differentiation to promote repair of barrier function after injury. The knowledge gained from these investigations will, in the short term, determine mechanisms by which CLDN18.1 can regulate human lung airway stem cells and contribute to repair of the cells lining an injured lung.
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