Research Areas

Syndecan-1 and Lung Repair

The goal of this project is to define basic mechanisms by which syndecan-1 regulates re-epithelialization in injured airway epithelium. We are identifying how syndecan-1 controls integrin activation, focal adhesion turnover and cell migration.

 

Syndecan-1 restrains cell migration by regulating focal adhesion turnover. From Altemeier et al. J Cell Sci. 2012;125:5188-5195.

Syndecan-1 and Influenza Infection

We are studying fundamental mechanisms by which syndecan-1 moderates lung inflammation after influenza infection. This research is determining how syndecan-1 regulates the airway epithelial response to influenza infection and limits lung injury through moderation of apoptosis.

 

Syndecan-1 attenuates lung inflammation after influenza infection. 

MicroRNAs and Chronic Allograft Rejection

This translational project has identified microRNA biomarkers that can segregate lung transplant patients with chronic allograft rejection from “normal” lung transplant recipients. The goals are to identify diagnostic modalities (i.e., biomarkers) for detecting chronic allograft rejection and to understand how microRNAs regulate the inflammatory and fibrotic responses in the lungs.

 

MicroRNA profiling of airway epithelium in vitro and in vivo revealed widespread differences in expression between conditions. From Chen P et al. Am J Pathol. 2013;183(5):1405–1410. 

TIMP-1 and Lung Injury

We previously found that TIMP-1 attenuates lung inflammation after LPS and bleomycin injury. We are now extending these initial studies to understand the mechanisms by which TIMP-1 is moderating the lung injury response.

 

 TIMP-1 is expressed in inflammatory and interstitial cells after lung injury. From Kim KH et al. Am J Respir Cell Mol Biol. 2005;33(3):271–279.

Dynactin-4 Polymorphisms and Pseudomonas Colonization in Cystic Fibrosis

This study is a multicenter collaboration with the Bamshad group at the University of Washington and the Schroer group at Johns Hopkins University. The Bamshad group identified two coding missense polymorphisms in dynactin-4 that are highly associated with pseudomonas colonization in cystic fibrosis patients. Working with Trina Schroer, who has studied dynactin for more than 15 years, we are attempting to understand how these polymorphisms regulate the lung innate immune response to pseudomonas infection.