Аннотация
The two principal features of airway goblet cells are rapid secretion of
mucin onto the airway surface and increase in number (hyperplasia) with
chronic inhaled `insult'. The first is associated with homeostasis, the
latter with pathophysiology. Myristoylated alanine-rich C kinase
(MARCKS) is a key molecule regulating mucin exocytosis, a process also
involving cooperative interaction between protein kinase (PK) C and PKG.
The epidermal growth factor (EGF) cascade and calcium activated chloride
channels (CLCA) are key signalling molecules involved in development of
goblet cell hyperplasia, with Bcl-2, an inhibitor of apoptosis, involved
in maintenance of hyperplasia. Goblet cell hyperplasia and associated
mucus hypersecretion is a pathophysiological feature of asthma and
chronic obstructive pulmonary disease (COPD). Novel therapeutic
strategies to prevent or reverse goblet cell hyperplasia include
inhibitors of EGF receptor tyrosine kinase and CLCA, of which viable
pharmaceutical molecules are now available for clinical trial in
hypersecretory conditions of the airways. (C) 2002 Elsevier Science Ltd.
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