Published ahead of print on May 12, 2005, doi:10.1165/rcmb.2005-0137OC Am. J. Respir. Cell Mol. Biol., Volume 33, Number 2, August 2005, 153-160 A more recent version of this article appeared on August 1, 2005
Submitted on April 13, 2005 Spontaneous Propagating Calcium Waves Underpin Airway Peristalsis in Embryonic Rat LungNeil C Featherstone1*,1 Division of Child Health, Royal Liverpool Children's Hospital (Alder Hey), University of Liverpool, Liverpool, Merseyside, United Kingdom, 2 School of Biological Sciences, University of Liverpool, Liverpool, Merseyside, United Kingdom, 3 The Physiological Laboratory, University of Liverpool, Liverpool, Merseyside, United Kingdom * To whom correspondence should be addressed. E-mail: N.C.Featherstone{at}Liverpool.ac.uk.
Prenatal airways from diverse species exhibit spontaneous peristaltic contractions (airway peristalsis). These contractile waves appear coupled to and may function to regulate prenatal lung growth. They are unaffected by atropine or tetrodotoxin but abolished by nifedipine. Nevertheless, the mechanisms by which these contractile waves are generated, regulated and propagated remain obscure. Using calcium imaging and whole embryonic lung organ culture, we demonstrate for the first time that peristalsis of the embryonic airway is driven by spontaneous, regenerative, temperature-sensitive calcium (Ca2+) waves. These Ca2+ waves propagate between individual airway smooth muscle cells coupled via gap junctions, are likely to be action potential mediated and are dependent on not only extracellular calcium entry via L-type voltage-gated channels but also intracellular calcium stores. Thus if airway peristalsis regulates lung growth, these findings mean that airway smooth muscle (ASM) Ca2+ waves in turn regulate prenatal lung morphogenesis.
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