Mortality of patients with chronic lung diseases continues to ncrease in the United States. Understanding the mechanisms of how the lung responds to injury and how this leads to abnormal lung healing is key to the development of novel therapeutic strategies to treat fibrotic diseases in the lung. The goal of our program at the Division of Pulmonary and Critical Care Medicine is to Division of Pulmonary and Critical Care Medicine of Northwestern University is to foster the career development of young investigators to focus on lung biology and to advance the understanding and treatment of pulmonary disorders. This interdisciplinary focus is reflected in the breadth of the lung disease research performed by our faculty members. Our program seeks to encourage young faculty to translate the rapid advances in molecular medicine to the bedside of patients with lung disease. To this goal, we are proposing this program to provide support for the hiring of new tenure-track faculty with a commitment to advancing their academic career;provide mentorship by senior investigators who are experts in their field;provide the laboratory facilities, foster collaborative relationships, and skilled supervision required for the advancement of independent investigators;and create an administrative structure that facilitates the new faculty's acquisition of independent extramural funding. To further the research in lung biology, we propose the recruitment of Dr. Lam to our Division. Dr. Lam is a new investigator who is collaborating with several investigators in the Division of Pulmonary and Critical Care Medicine of Northwestern University and providing some ofthe seminal research in understanding the role of the canonical Wnt/p-catenin pathway in adult lung response to injury and repair. The Division of Pulmonary and Critical Care Medicine of Northwestern University is a center for innovative research into the mechanisms of lung injury, the addition of Dr. Lam and her research on the role p-catenin signaling in abnormal wound repair will not only complement but also elevate the scientific capacity of the Division. Understanding the mechanisms by which p-catenin signaling effects fibroproliferative diseases in the lung will have significant impact not only upon the understanding of fundamentals lung biology but also upon strategies for treatment and prevention of these devastating diseases. Lung diseases are on the rise in the United States and around the world. Understanding how the lung responds to injury and how aberrant healing leads to lung scarring is vital in order to develop preventive and treatment measures. To this goal, new investigators need to be recruited to develop collaborative, multidisciplinary research that will facitlitate rapid advances in molecular medicine to the bedside.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Center Core Grants (P30)
Project #
1P30HL101292-01
Application #
7858936
Study Section
Special Emphasis Panel (ZHL1-CSR-E (O1))
Program Officer
Rothgeb, Ann E
Project Start
2009-09-30
Project End
2011-08-31
Budget Start
2009-09-30
Budget End
2010-08-31
Support Year
1
Fiscal Year
2009
Total Cost
$440,700
Indirect Cost
Name
Northwestern University at Chicago
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
005436803
City
Chicago
State
IL
Country
United States
Zip Code
60611
Sennello, Joseph A; Misharin, Alexander V; Flozak, Annette S et al. (2017) Lrp5/?-Catenin Signaling Controls Lung Macrophage Differentiation and Inhibits Resolution of Fibrosis. Am J Respir Cell Mol Biol 56:191-201
Flozak, Annette S; Lam, Anna P; Gottardi, Cara J (2016) A Simple Method to Assess Abundance of the ?-Catenin Signaling Pool in Cells. Methods Mol Biol 1481:49-60
Reinke, Lauren; Lam, Anna P; Flozak, Annette S et al. (2016) Adiponectin inhibits Wnt co-receptor, Lrp6, phosphorylation and ?-catenin signaling. Biochem Biophys Res Commun 470:606-612
Lam, Anna P; Herazo-Maya, Jose D; Sennello, Joseph A et al. (2014) Wnt coreceptor Lrp5 is a driver of idiopathic pulmonary fibrosis. Am J Respir Crit Care Med 190:185-95
Kamp, David W; Liu, Gang; Cheresh, Paul et al. (2013) Asbestos-induced alveolar epithelial cell apoptosis. The role of endoplasmic reticulum stress response. Am J Respir Cell Mol Biol 49:892-901
Wei, Jun; Melichian, Denisa; Komura, Kazuhiro et al. (2011) Canonical Wnt signaling induces skin fibrosis and subcutaneous lipoatrophy: a novel mouse model for scleroderma? Arthritis Rheum 63:1707-17
Lam, Anna P; Gottardi, Cara J; Tuder, Rubin (2011) Regenerative pathways and emphysema: a new paradigm? Am J Respir Crit Care Med 183:688-90
Lam, Anna P; Flozak, Annette S; Russell, Susan et al. (2011) Nuclear ?-catenin is increased in systemic sclerosis pulmonary fibrosis and promotes lung fibroblast migration and proliferation. Am J Respir Cell Mol Biol 45:915-22
Lam, Anna P; Gottardi, Cara J (2011) ?-catenin signaling: a novel mediator of fibrosis and potential therapeutic target. Curr Opin Rheumatol 23:562-7
Flozak, Annette S; Lam, Anna P; Russell, Susan et al. (2010) Beta-catenin/T-cell factor signaling is activated during lung injury and promotes the survival and migration of alveolar epithelial cells. J Biol Chem 285:3157-67

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