Follicle-stimulating hormone receptor and its messenger ribonucleic acid are present in the bovine cervix and can regulate cervical prostanoid synthesis
D. Mizrachi et M. Shemesh, Follicle-stimulating hormone receptor and its messenger ribonucleic acid are present in the bovine cervix and can regulate cervical prostanoid synthesis, BIOL REPROD, 61(3), 1999, pp. 776-784
The hypothesis that FSH regulates the bovine cervical prostaglandin E-2 (PG
E(2)) synthesis that is known to be associated with cervical relaxation and
opening at the time of estrus was investigated. Cervical tissue from pre-e
strous/estrous, luteal, and postovulatory cows were examined for 1) the pre
sence of bovine (b) FSH receptor (R) and its corresponding mRNA and 2) the
effect of FSH on the PGE(2) regulatory pathway in vitro. The presence of bF
SHR mRNA in the cervix (maximal during pre-estrus/estrus) was demonstrated
by the expression of a reverse transcription (RT) polymerase chain reaction
(PCR) product (384 base pairs) specific for bFSHR mRNA and sequencing. Nor
thern blotting revealed three transcripts (2.5, 3.3, and 3.8 kilobases [kb]
) in cervix from pre-estrous/estrous cows. The level of FSHR (75 kDa) was s
ignificantly higher (p < 0.01) in Western blots of pre-estrous/estrous cerv
ix than in other cervical tissues. There was a good correlation between the
75-kDa protein expression and its corresponding transcript of 2.55 kb thro
ughout the estrous cycle as described by Northern blot analysis as well as
RT-PCR. Incubation of FSH (10 ng/ml) with pre-estrous/estrous cervix result
ed in a 3-fold increase in the expression of FSHR and a 2-fold increase in
both G protein (alpha(s)) and cyclooxygenase II. FSH (5-20 ng/ml) significa
ntly increased(p < 0.01) cAMP, inositol phosphate (p < 0.01), and PGE(2) (p
< 0.01) production by pre-estrous/estrous cervix but not by cervix at the
other stages, We conclude that bovine cervix at the time of the peripheral
plasma FSH peak (pre-estrus/estrus) contains high levels of FSHR and respon
ds to FSH by increasing the PGE(2) production responsible for cervical rela
xation at estrus.