Regulation of AMPK Function by CFTR in human airway cells

Description of projects available to graduate students:
Recent results suggest that the metabolic sensor AMP-activated kinase (AMPK) is activated in cystic fibrosis (CF) airway epithelial cells relative to non-CF cells. Recent work has focused on the mechanism for AMPK activation and the role of this activation in the excessive inflammatory state present in the CF airway. AMPK activation both inhibits the secretion of pro-inflammatory cytokines and excessive epithelial Na channel activity in primary human bronchial epithelial cells. Further pharmacological activation of AMPK, by countering these processes, thus represents a novel potential therapeutic strategy for the treatment of CF lung disease. Pre-clinical studies are underway to test whether FDA-approved AMPK activators are of benefit in CF airway cells.

Techniques graduate student will learn:
Ussing chamber short-circuit current measurements, viral transduction, Western blotting, multiplex cytokine analysis, RNA interference, cell culture