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J. Biol. Chem., Vol. 277, Issue 48, 46447-46455, November 29, 2002
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From the Departments of Previous studies indicated that calcitonin
(CT), a peptide hormone involved in calcium homeostasis, is transiently
expressed in the receptive rat and human endometrial epithelia within
the window of implantation. Attenuation of uterine CT expression using antisense methods severely impaired implantation in the rat. The molecular pathway of CT in the pregnant uterus, however, remains unknown. In the present study, we investigated the cellular events following the binding of CT to its membrane receptors in human endometrial epithelial cell line Ishikawa. We observed that CT treatment triggers a transient rise in intracellular calcium in these
cells. Most interestingly, CT treatment also led to the disappearance
of E-cadherin, a critical cell adhesion molecule, from cell-cell
contact sites. Blockade of intracellular calcium release by BAPTA-AM
(1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl) prevented the CT-induced disappearance of E-cadherin. Our studies further revealed that CT treatment markedly down-regulates the level of E-cadherin mRNA in Ishikawa cells. We
also examined whether CT influences the expression of E-cadherin mRNA in intact rat uterine tissue during implantation. In pregnant rats, high levels of E-cadherin mRNA were expressed during the first 3 days of gestation when the CT mRNA in uterine epithelial cells is undetectable. Concomitant with a transient burst of CT expression during days 4-5 of pregnancy, the level of E-cadherin mRNA declined sharply. Furthermore, administration of exogenous CT
to animals on day 2 of pregnancy led to a premature suppression of
E-cadherin mRNA level on day 3, indicating a direct link between elevated levels of uterine CT and the down-regulation of E-cadherin expression in the surface epithelium. Collectively, our results are
consistent with the hypothesis that CT-induced reduction in E-cadherin
expression may remodel the adherens junctions between epithelial cells,
and this change in epithelial cell phenotype might be a critical event
during the implantation of the blastocyst.
Calcitonin Down-regulates E-cadherin Expression in Rodent Uterine
Epithelium during Implantation*
,
, and Veterinary Biosciences and
¶ Molecular and Integrative Physiology, University of Illinois at
Urbana-Champaign, Urbana, Illinois 61802 and the
§ Department of Obstetrics and Gynecology, C. S. Mott
Center for Human Growth and Development, Wayne State University School
of Medicine, Detroit, Michigan 48201
*
This work was supported in part by National Institutes of
Health Grants R01 HD-34527 and R01 HD-39291 (to I. C. B.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by National Institutes of Health Grants R01-DK-50257
and U54-HD-13541.
**
To whom correspondence should be addressed: Dept. of Veterinary
Biosciences, University of Illinois at Urbana-Champaign, 3641 VMBSB,
2001 S. Lincoln, Urbana, IL 61802. Tel.: 217-333-7986; Fax:
217-244-1652; E-mail: ibagchi@uiuc.edu.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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