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Abstract
Several previous studies have demonstrated that uterine
Cox2 (also known as Ptgs2) is required for
implantation. Luteinizing hormone (LH) released from
anterior pituitary gland and human chorionic gonadotropin
released from placenta (hCG), can upregulate the uterine
Cox2 gene expression. The Lhcgr knockout
(herein designated LHRKO) animals have implantation
failure even after estradiol and progesterone therapy.
These findings led us to investigate the dependence of
uterine Cox2 gene expression on LH signaling in
LHRKO animals. The results revealed that while Cox2
(also known as Ptgs2) mRNA levels were similar,
Cox2 mRNA levels were lower in uterus of null
animals than in wild-type siblings. Treatment with hCG did
not increase Cox2 mRNA levels in null endometrial
stromal or myometrial smooth muscle cells, unless gene
therapy was performed to introduce native LHCGR. The
Cox2 mRNA levels, on the other hand, did not change
regardless of the introduction of native or activated
Lhcgr or hCG treatment. The Cox2 mRNA increase
paralleled the cAMP raise, suggesting that LH uses the
cAMP second messenger system. Treating the wild-type
uterine cells with hCG, resulted in a Cox2, but not
Cox2 mRNA increase. This increase became
exaggerated when additional native LHCGR were introduced
by gene therapy. In conclusion, deletion and reinsertion
of Lhcgr further support that uterine Cox2
gene expression is dependent on LH signaling.
Key words:
Female Reproductive Tract
Cyclic adenosine monophosphate
Gene regulation
Luteinizing hormone
Uterus
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