Petr Bachan, MD

Mentor:  David H. Ingbar, MD

Education:     1986 – 1992, M.D., Masaryk University
                            Medical School, Czech Republic
                      1992 - 1995, Anesthesiology Residency,
                            National Oncology Institute, Bratislava,
                            Slovak Republic
                      1995 - 1998, Internal Medicine Residency,
                            Henry Ford Hospital, Detroit, MI
                      2006 – Present, Pulmonary/Critical Care
                            Fellow, University of Minnesota

Project Summary:

My objective is to study the alveolar epithelial cell migration component of repair from acute lung injury. The repair process from acute lung injury (ALI) requires that a pool of alveolar type II (AEC II) or progenitor cells restore the alveolus by a combination of proliferation, adhesion, spreading, and migration. The underlying rationale for this project is that understanding the molecular mechanisms of AEC migration will permit therapeutic interventions to speed lung repair.

Migration over denuded basement membrane or on hyaline membranes (provisional matrix) is an essential step in this process.  Gene expression and protein analysis of pathways involved in migration will be tested. The ultimate goal is to identify potential sites amenable to therapeutic interventions which will eventually lead to improved outcome of patients with acute lung injury.   

Specific aims are:

Aim 1. To determine the effects of hyperoxia on AEC adhesion and migration on fibronectin.   Adhesion and migration of alveolar type II cells (AEC II) is adversely affected during the cell stress as modeled by hyperoxic injury, but rebounds to supranormal levels during recovery. Hyperoxic injury induces cell arrest by growth arrest gene gas-1 upregulation. Early cell cycle genes c-fos, c-jun ,jun B and integrin downstream signaling molecules FAK, PI3K, PTEN, JNK, Rac, VEGF are downregulated immediately after injury, but expression will increase after 24h of recovery.

Aim 2.  To determine whether overexpression and inhibition of alpha5beta1 integrin regulate migration on fibronectin of AECs II in normoxia, after 24h of hyperoxia, and after 24h recovery from hyperoxia. 

Grants Submitted:  American Lung Association (local/regional) Research Fellowship

Last Updated 2/22/2008