Immunolocalization of the mnav2.3 na+ channel in mouse heart:
upregulation in myometrium during pregnancy.
Knittle, Timothy J., Kelly L. Doyle, and Michael M. Tamkun.
Departments of Molecular Physiology and Biophysics and
Pharmacology, Vanderbilt University School of Medicine, Nashville, TN
37232
APStracts 2:0324C, 1995.
mNav2.3 is a putative voltage-dependent sodium channel (NaCh) gene
expressed in both mouse heart and uterus that shares only 45% amino
acid identity with NaChs from gene subfamily 1. Immunofluorescence
studies, using polyclonal antibodies against two distinct epitopes,
revealed that mNav2.3 protein in heart colocalized with nerve
-specific antibody binding. Similar mNav2.3- specific antibody
staining was observed in virgin uterus. However, mNav2.3 expression
in uterine nerve disappeared during late pregnancy concurrent with an
appearance in both the longitudinal and circular uterine smooth
muscle, which reached a maximum at term and quickly declined within
two days postpartum. mNav2.3 expression in term uterus often
colocalized on the myocyte surface with connexin 43. The
immunofluorescence results are supported by Western analysis in which
the 217 kD NaCh increased during late pregnancy and declined two days
postpartum. These data provide perhaps the most dramatic example of
NaCh channel regulation. The acute and transient up regulation in
myometrium during gestation suggests the Nav2.3 channel plays a role
in uterine function at term.
Received 11 May 1995; accepted in final form 8 August 1995.
APS Manuscript Number C248-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.