Stephen Land

Lung development, and the closely related process of lung repair, depend on time and location dependent expression of growth factors, receptors and antagonists which regulate the proliferation of lung stem cells and the formation of branched airway and vascular structures. Disruption of this signalling network by, for example, changes in lung oxygenation caused by premature delivery, hypoxia/asphyxia or infection can lead to life-long respiratory complications which may significantly limit life-span and quality. Our major interest is to determine the relationship between environmental factors (for example, oxygen, free radical production, bacterial infection) which may influence lung morphogenesis in the fetus and the prospects of lung re-growth during childhood and adult life. Our research activities are currently focussed on three themes:

The oxygen dependence of lung morphogenesis:

The lung develops in utero at a Po2 equivalent to that at the summit of Mt. Everest (~23-30mmHg), yet must develop to perform the gas exchange at the highest systemic Po2 (100mmHg) following birth. We are examining the oxygen dependency of factors responsible for lung growth and lung cell differentiation to determine how oxygen availability modulates the process of lung development pre- and post-term.

Regulation of lung morphogenesis by bacterial endotoxins:

Although infection of the fetal membranes during pregnancy may result in premature delivery and subsequent respiratory distress, lipopolysaccharides (endotoxins) shed from the bacterial cell wall actively promote the process of lung maturation in utero. Our studies examine the relationship between these endotoxins and the genes that are involved in regulating airway growth and surfactant production.

Oxygen conformance of lung cells:

The ability to regulate ATP synthesis and demand during dynamic shifts in oxygen tension depends on an innate ability to sense and respond to changes in oxygen tension before conditions threaten cell viability. We are examining the mechanisms that regulate respiratory chain activity in response to changes in oxygen tension and which signalling pathways are involved in co-ordinating changes in the rates of dominant ATP demanding cell processes (e.g. Na+ pumping; protein translation).

Publications

Maintained by: H Murphie.

The University of Dundee is a Scottish Registered Charity, No.SC015096

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