Shutang Zhou

Shutang Zhou

Shutang Zhou, PhD
Assistant Professor, Department of Pathology
Duke University, USA

Biography

Shutang Zhou received his Ph.D. at Queen’s University, Canada in 2003. He is currently an assistant professor at Duke University Medical Center. He has 11 peer-reviewed papers and 1 patent. He has recently investigated the novel functions for neuronal PAS domain protein 3 (NPAS3) and the neuropeptide GRP in lung development and/or chronic lung disease. Two major discoveries he has recently made are: (1) NPAS3 is the functional mammalian homolog of trachealess, the master regulator of Drosophila respiratory system; and (2) GRP mediates immediate and delayed airway hyperreactivity and airway inflammation in asthma. GRP blockade prevents airway inflammation, cytokine production, and airway hyperreactivity in two mouse models of asthma. These discoveries have resulted in 2 papers published in Proceedings of the National Academy of Sciences USA.

Research Interest

My major research interest is to identify molecular mechanisms and signaling pathways of lung development and chronic lung diseases, with emphasis on two distinct pathways:
(1) Neuronal bHLH-PAS transcription factor NPAS3. Our data demonstrate that NPAS3 is the functional mammalian homolog of trachealess, the master regulator of the Drosophila respiratory system. Studies are being conducted to further elucidate the cellular and molecular mechanisms of lung development regulated by NPAS3, to determine how NPAS3 deficiency might contribute to emphysema and asthma, and to identify the role of NPAS3 in lung cancer. (2) Neuropeptides, immunity and asthma. In both ozone and OVA models, the gastrin-releasing peptide (GRP) blockade abrogates AHR and bronchoalveolar lavage (BAL) macrophages and granulocytes, and also decreased BAL levels of cytokines implicated in asthma. Thus, GRP mediates airway hyperreactivity and airway inflammation in mice, suggesting that GRP blockade is promising as a broad-spectrum therapeutic approach to treat and/or prevent asthma in humans. We are now investigating the critical target cells for primary effects of GRP and the signaling pathways transducing these effects. We anticipate direct effects on airway smooth muscle, macrophages, and T cells, leading to in-depth analyses of immunoregulation by the multifunctional G protein-coupled GRP receptor.