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J. Biol. Chem., Vol. 275, Issue 51, 40252-40257, December 22, 2000
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From the Departments of Obstetrics/Gynecology and Cell Biology and
Physiology, Washington University School of Medicine, St. Louis,
Missouri 63110
We report that a decrease in facilitative glucose
transporter (GLUT1) expression and reduced glucose transport trigger
apoptosis in the murine blastocyst. Inhibition of GLUT1
expression either by high glucose conditions or with antisense
oligodeoxynucleotides significantly lowers protein expression and
function of GLUT1 and as a result induces a high rate of apoptosis at
the blastocyst stage. Similar to wild-type mice, embryos from
streptozotocin-induced diabetic Bax
Decreased Glucose Transporter Expression Triggers
BAX-dependent Apoptosis in the Murine Blastocyst*
, and
/ mice experienced
a significant decrease in glucose transport compared with embryos from
non-diabetic Bax / mice. However, despite this
decrease, these blastocysts demonstrate significantly fewer apoptotic
nuclei as compared with blastocysts from hyperglycemic wild-type mice.
This decrease in preimplantation apoptosis correlates with a decrease
in resorptions and malformations among the infants of the hyperglycemic
Bax / mice versus the Bax +/+
and +/ mice. These findings suggest that hyperglycemia by decreasing
glucose transport acts as a cell death signal to trigger a
BAX-dependent apoptotic cascade in the murine blastocyst. This work also supports the hypothesis that increased apoptosis at a
blastocyst stage because of maternal hyperglycemia may result in loss
of key progenitor cells and manifest as a resorption or malformation,
two adverse pregnancy outcomes more common in diabetic women.
*
This work was supported in part by the National Institutes
of Health Grants R03 HD34693 and P60 DK30579 (to K. H. M).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.
Recipient of a National Institutes of Health Postdoctoral
Fellowship Grant T32-DK38496-20.
§
Recipient of a Burroughs Wellcome Fund Career Award in the
Biomedical Sciences and a Juvenile Diabetes Fund Research Award. To
whom correspondence should be addressed: Dept. of Ob/Gyn, 4911 Barnes-Jewish Hospital Plaza, 6th Floor Maternity, St. Louis, MO 63110. Tel.: 314-362-1765; Fax: 314-362-3328; E-mail: moleyk@ msnotes.wustl.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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