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Physiology Home > People > Faculty >
Gu
Most of the sensory inputs arising from airways and lungs are conducted in vagus nerves and their branches. It is known that >75% of vagal bronchopulmonary afferents are non-myelinated (C-) fibers. Hypersensitivity of these C-fiber afferents plays an important role in the development of airway hyperresponsiveness associated with airway mucosal injury or inflammation. Our primary interest is to uncover the neurogenic mechanisms involved in pulmonary pathophysiological conditions such as asthma, lung carcinoma and chronic obstructive pulmonary disease (COPD), and therefore to offer new therapeutic strategies for the treatment of these respiratory diseases. Electrophysiological and pharmacological approaches, cell- and molecular-biology techniques are used in our laboratory. Recent publications: Gu Q, Lee, LY. Regulation of acid signaling in rat pulmonary sensory neurons by protease-activated receptor-2. Am J Physiol Lung Cell Mol Physiol 298: L454-461, 2010. Gu Q, Lin RL. Heavy metals zinc, cadmium and copper stimulate pulmonary sensory neurons via direct activation of TRPA1. J Appl Physiol 108: 891-897, 2010. Gu Q, Lee LY. Acid-sensing ion channels and pain. Pharmaceuticals 3: 1411-1425, 2010. Open access: http://www.mdpi.com/1424-8247/3/5/1411/ Gu Q, Lee LY. Effect of PAR2 activation on single TRPV1 channel activities in rat vagal pulmonary sensory neurons. Exp Physiol 94: 928-936, 2009. Gu Q, Lim ME, Gleich GJ, Lee LY. Mechanisms of eosinophil major basic protein-evoked hyperexcitability of vagal pulmonary chemosensitive neurons. Am J Physiol Lung Cell Mol Physiol 296: L453-461, 2009. |
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