June 16, 2009 In the normal lung, the airways are lined by a
balanced mixture of ciliated, secretory and neuroendocrine cells
which perform functions as diverse as air humidification,
detoxification, and clearance of environmental particles. This
balance can be altered dramatically by faulty adaptation
responses of the lung to cigarette smoke or allergens in
patients with Chronic Obstructive Pulmonary Disease (COPD) and
asthma. How these different cell types emerge from lung
progenitor cells and how these fates are balanced in developing
airways, remain an open question. A study from a research team
led by Wellington Cardoso, MD, a professor at the Pulmonary
Center Boston University School of Medicine and Director of the
Program in Lung Development and Progenitor Cell Biology, sheds
light into this problem. The Notch pathway is a major regulator
of cell fate decisions in developing cells from fruit flies to
humans. Using mouse genetic models, the BU researchers
inactivated Notch signaling in the lung and disc