Research

Ji, James, M.D., M.S.

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Contact: james.ji@uthct.edu

Research Interest:

Regulation of pulmonary epithelial salt and fluid transport

Grant Funding:

Regulation of lung epithelial sodium channel by cGMP. NHLBI, HL087017 (PI).

Current Projects:

  • Posttranslational regulation of lung epithelial sodium channels by reactive species and cGMP.
  • Salt and fluid transport at the cellular and molecular levels in bacteria and virus-induced pulmonary edema and acute lung injuries.
  • Regulation of mucus clearance in inflammatic airway associated with asthma, chronic obstructive pulmonary disease (COPD), allergy, cigarette smoke, and occupational lung diseases.
  • Physiological and pathogenic roles of pulmonary ENaC and interactions with fibrinolytic cascades.

Research Overview:

Epithelial sodium channel (ENaC) plays a critical role in airway mucus clearance and alveolar fluid clearance. Dysfunctional mucus/fluid clearance has been implicated in the pathogenesis of various critical pulmonary diseases/injuries, for instance, Cystic fibrosis, Pseudohypoaldosteronism type 1 (PHA-1), viral and bacterial pneumonia, influenza, occupational/environmental bronchitis, chronic obstructive pulmonary disease (COPD), and allergic respiratory disorders. ENaC as a major pathway for fluid resolution contributes up to 70% of lavage/fluid clearance. ENaC activity is regulated by post-translational modifications, including proteolysis and glycosylation. Our studies on the regulation of ENaC function in lung epithelium will provide novel information to our understanding of the pathogenesis of edematous and hypersecretive pulmonary diseases.

Selected Papers:

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