Research Focus

My lab studies the mechanisms that govern airway repair after injury and how inappropriate repair proceeds to airway fibrosis. A major focus has been basic research into mechanisms regulating airway epithelial cell migration using in vitro and in vivo mouse models of airway injury. Specifically, we have worked on understanding how matrix metalloproteinases (in particular MMP7) facilitate re-epithelialization after injury. Our research has now led us to study how syndecan-1 regulates cell-matrix interactions as the airway epithelium migrates over a wound. Additionally, my lab has another line of investigation into how microRNAs participate in airway repair and fibrosis. This project takes a translational approach by using human airway epithelial cells procured from lung transplant patients. Our goal is to identify putative microRNAs that participate in the pathophysiology of chronic rejection after lung transplantation (i.e., obliterative bronchiolitis).

Relevant Publications

Chen P, Farivar AS, Mulligan MS, Madtes DK. TIMP-1 Deficiency Abrogates Obliterative Airway Disease after Heterotopic Tracheal Transplantation. Amer J. Resp. Cell Mol. Biol 2006 ; 34(4) :464-472. (PMID: 16388023)

Chen P, McGuire JK, Hackman RC, Kim KH, Black RA, Poindexter K, Yan W, Liu P, Chen AJ, Parks WC, Madtes DK. Tissue Inhibitor of Metalloproteinase-1 Moderates Airway Re-epithelialization by Regulating Matrilysin Activity. Am J Pathol. 2008; 172:1256-70. (PMID: 18385523)

Chen P, Parks WC. The Role of Matrix Metalloproteinases in Epithelial Cell Migration. J Cell Biochem. 2009; 108:1233-43. (PMID: 19798678)

Chen P, Abacherli LA, Nadler ST, Wang Y, Li Q, Parks WC. Matrilysin Shedding of Syndecan-1 Facilitates Re-epithelialization by Affecting a2b1 Integrin Activation. PLoS ONE. 2009. 4(8): e6565. (PMID: 19668337)

Active Funding