Stimulation of surfactant lipid secretion from fetal type ii
pneumocytes by gastrin-releasing peptide.
Asokananthan, N., and Max H. Cake.
School of Biological and Environmental Sciences, Murdoch
University, Murdoch, Western Australia, 6150
APStracts 2:0170L, 1995.
Gastrin-releasing peptide and bombesin apparently enhance the rate of
secretion of surfactant lipids from cultured fetal rat type II
pneumocytes. This effect, evident within one hour of addition of the
peptide, is concentration-dependent with a maximal response at 3.0
nM. When the effect of GRP was assessed in comparison with other
known secretagogues, it was found that whereas GRP and isoproterenol
were additive in their effect, there was no response to GRP in the
presence of saturating concentrations of A23187 or phorbol 12
-myristate 13-acetate. This suggests that the secretory response to
GRP is via activation of Ca2+/calmodulin-dependent protein kinase
and/or protein kinase C and is independent of cyclic AMP-dependent
protein kinase. This conclusion is supported by the observation that
the GRP-induced secretion is inhibited by calphostin C, an inhibitor
of protein kinase C, but not by H89, an inhibitor of cyclic AMP
-dependent protein kinase. The fact that GRP regulates surfactant
secretion from type II pneumocytes suggests that it and/or related
peptides may play a significant role in the physiological maturation
of the lung.
Received 21 February 1995; accepted in final form 11 September
1995.
APS Manuscript Number L52-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 31 October 95