The lab is focused on basic and biomedical aspects of lung injury and matrix remodeling. The PI has a long history of investigation of proteolytic systems involved in this process, especially the urokinase receptor and endosomal cysteine proteases. Currently, the lab is focused on two major problems: airway epithelial to mesenchymal transition (EMT) in the lung in the context of injury, including emphysema, and integrin signaling in lung cancer. Our focus in EMT is its regulation by beta 1 integrins, mediated indirectly through the influence of integrins on signaling pathways that underlie EMT, such as TGF beta 1. We remain interested in expression of the urokinase receptor (uPAR) and its interaction with integrins because this appears to influence integrin signaling and the migratory potential of epithelial cells, relevant to repair and metastasis. UPAR has also been implicated in EMT. Various current projects in the lab explore the degree of EMT in the lung following injury, the influence of selective integrin null mice on epithelial cell responses to injury, and regulation of integrin signaling by the urokinase receptor. Our focus in lung cancer is the role of uPAR/integrin interactions in empowering metastasis. Here we are using transgenic mice as a model for experimental lung cancer as well as single cells isolated from primary human lung tumors. More detailed descriptions of current projects related to EMT, emphysema, and lung cancer, current lab members, and recent publications, are provided within the website (pulmonary.ucsf.edu/chapmanlab).