Wu-Lin Zuo

TL;DR: Analysis of the airway epithelium revealed that EGFR is enriched in airway BCs, whereas its ligand EGF is induced by smoking in ciliated cells, suggesting that activation of EGFR in airways BCs by smoking-induced EGF represents a unique mechanism whereby smoking can alter airwayhelial differentiation and barrier function.

TL;DR: Novel insights are provided into the molecular phenotype and biologic functions of the human club cell population and basal cells are identified as the human progenitor cells for club cells.

TL;DR: Smoking‐induced global distal‐to‐proximal reprogramming of the SAE represents a novel pathologic feature of COPD and is mediated by exaggerated epidermal growth factor/epidermalgrowth factor receptor signaling in SAE BCs.

TL;DR: EGF‐AREG interplay in airway BC stem/progenitor cells is one of the mechanisms that mediates the interconnected pathogenesis of all major smoking‐induced lesions in the human airway epithelium.

TL;DR: The results suggest that ATP inhibition of vas deferens smooth muscle contraction is epithelium dependent, and suggests that ATP activates P2Y receptor‐coupled Ca2+ mobilization leading to the release of PGE2 from epithelial cells, which in turn activates cAMP‐dependent K+ channels in smooth muscle cells leads to the hyperpolarization of membrane voltage and the inhibition of Vas deferen contraction.