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Molecular Human Reproduction, Vol. 8, No. 8, 758-764, August 2002
© 2002 European Society of Human Reproduction and Embryology

Embryology

Expression of cystic fibrosis transmembrane conductance regulator during early human embryo development

Avraham Ben-Chetrit1,*, Monica Antenos1,*, Andrea Jurisicova1, Eva A. Pasyk3, David Chitayat2, J.Kevin Foskett3,4 and Robert F. Casper1,5,5

1 Division of Reproductive Sciences, Department of Obstetrics and Gynaecology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 2 Prenatal Diagnosis Program, the Toronto Hospital General Division, 3 Division of Cell Biology, 4 Department of Biochemistry, The Hospital for Sick Children and 5 Department of Physiology, University of Toronto, M5G 1X8, Ontario, Canada

Formation of the blastocyst is one of the first morphological changes in early embryonic development. Ion transport has been shown to be crucial for blastocoele cavity formation and expansion, although the mechanisms that underlie this process are presently unknown. As a transmembrane Cl- channel, the cystic fibrosis transmembrane conductance regulator (CFTR) may participate in ion transport and early blastocoele formation. CFTR mRNA was detected throughout preimplantation embryo development and in the unfertilized oocyte. Immunocytochemistry disclosed the presence of CFTR protein from the 8-cell stage, reaching maximum immunoreactivity at early blastocyst stage embryos. Patch clamp electrophysiology of morulae and blastocysts demonstrated typical CFTR Cl- channel activities in the apical membrane of trophectoderm cells. Thus CFTR is expressed both at mRNA and protein levels in human morulae and blastocysts, and functions as a cAMP-regulated apical membrane Cl- channel. These data suggest that CFTR may contribute to blastocoele formation in the early human embryo.

blastocoele/blastocyst/CFTR/cystic fibrosis/embryo cavitation

5 To whom correspondence should be addressed at: 600 University Ave, Room 876, Toronto, Ontario M5G 1X5, Canada. E-mail: r.casper{at}utoronto.ca

* These authors contributed equally to this work.


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