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Pediatrics / Pediatric Research Newsletter / April 2010 / Jennifer Murzycki, MD, PhD

April 2010 Newsletter

Jennifer Murzycki, M.D., Ph.D.

Dr. Murzycki, is investigating the role of Proline Rich Tyrosine Kinase 2 (PYK2) in the Pulmonary Response to Mechanical Strain. Acute lung injury (ALI)and acute respiratory distress syndrome (ARDS) are responsible for significant morbidity and mortality in the United States. Mechanical strain from ventilation is a major contributing factor to this disease process. The protein signaling pathways by which the lung epithelium responds to and heals from these diseases is still not well understood. Proline rich tyrosine kinase 2 (PYK2) has previously been shown to be involved in the signaling pathways responsible for cellular migration and differentiation in several tissues in the human body.  In hematopoietic cell lines, PYK2 appears to be involved in both myeloid and lymphoid cell migration to areas of infection and inflammation.  PYK2 has also been shown to have a role in endothelial cell migration during angiogenesis, and has variable expression in several types of cancer. Focal adhesion kinase (FAK), is a tyrosine kinase in the same family as PYK2. The two often play similar roles in signaling pathways.  FAK mediates cell signaling in alveolar type 2 cells undergoing mechanical ventilation. We hypothesize that given the similarity between FAK and PYK2, PYK2 may play a unique role in alveolar type 2 cell responses to strain. Murzycki’s current work focuses on determining if PYK2 is present in pulmonary alveolar epithelium and how its expression is modulated when epithelial cells undergo mechanical strain, similar to that experienced during mechanical ventilation. Cultured pulmonary epithelial cells will be strained in vitro, and mice ventilated in vivo. PYK2 protein will be assessed in both the cultured and native pulmonary epithelium by western blot and immunohistochemistry respectively. While studies to date have indicated that PYK2 may play a role in cancer migration in the lung, no studies have shown an alteration in the expression of PYK2 related to mechanical strain in the lung. This study aims to elucidate a novel role for PYK2 by demonstrating its involvement in pulmonary strain independent of malignancy. This will provide insights into the signaling pathways that are responsible for the cellular responses observed in mechanical strain, which contributes to ALI and ARDS.