start-ver=1.4
cd-journal=joma
no-vol=28
cd-vols=
no-issue=10
article-no=
start-page=1588
end-page=1597
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=201504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Genomic and non-genomic effects of progesterone on prostaglandin (PG) F2α and PGE2 production in the bovine endometrium
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= Progesterone (P4) acts through different actuating pathways called genomic and non-genomic pathways. Here we investigated whether P4 regulates prostaglandin (PG) F2? (PGF) and PGE2 production in bovine endometrium through different pathways. Cultured endometrial cells were exposed to P4 for a short time (5-20min) or bovine serum albumin (BSA)-conjugated P4 (P4-BSA) for 24h. Progesterone treatment for 24h stimulated PGE2 production in epithelial cells, but suppressed both PGF and PGE2 production and the expression of PG-metabolising enzymes including phospholipase A2 (PLA2) and cyclooxygenase-2 (COX2) in stromal cells. Short-term (5-20min) P4 treatment did not affect PLA2 or COX2 transcript levels in either cell type. P4-BSA increased PGF and PGE2 production only in epithelial cells. Nuclear P4 receptor mRNA expression in endometrium was higher at the follicular phase than at the early- to mid-luteal stages, whereas membrane P4 receptor mRNA expression did not change throughout the oestrous cycle. The overall results suggest that P4 controls PG production by inhibiting enzymes via a genomic pathway and by stimulating signal transduction via a non-genomic pathway. Consequently, P4 may protect the corpus luteum by attenuating PGF production in stromal cells and by increasing PGE2 secretion from epithelial cells
en-copyright=
kn-copyright=

en-aut-name=KuseMariko
en-aut-sei=Kuse
en-aut-mei=Mariko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakumotoRyosuke
en-aut-sei=Sakumoto
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OkudaKiyoshi
en-aut-sei=Okuda
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Laboratory of Reproductive Physiology, Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Reproductive Biology Research Unit, National Institute of Agrobiological Sciences
kn-affil=

affil-num=3
en-affil=Laboratory of Reproductive Physiology, Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=cows
kn-keyword=cows
en-keyword=luteolysis
kn-keyword=luteolysis
en-keyword=steroid hormone
kn-keyword=steroid hormone
en-keyword=uterus
kn-keyword=uterus
END

start-ver=1.4
cd-journal=joma
no-vol=28
cd-vols=
no-issue=10
article-no=
start-page=1479
end-page=1486
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=201505
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Multiple roles of hypoxia in ovarian function: roles of hypoxia-inducible factor-related and -unrelated signals during the luteal phase
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract= There is increasing interest in the role of oxygen conditions in the microenvironment of organs because of the discovery of a hypoxia-specific transcription factor, namely hypoxia-inducible factor (HIF) 1. Ovarian function has several phases that change day by day, including ovulation, follicular growth and corpus luteum formation and regression. These phases are regulated by many factors, including pituitary hormones and local hormones, such as steroids, peptides and cytokines, as well as oxygen conditions. Hypoxia strongly induces angiogenesis because transcription of the potent angiogenic factor vascular endothelial growth factor (VEGF) is regulated by HIF1. Follicular development and luteal formation are accompanied by a marked increase in angiogenesis assisted by HIF1-VEGF signalling. Hypoxia is also one of the factors that induces luteolysis by suppressing progesterone synthesis and by promoting apoptosis of luteal cells. The present review focuses on recent studies of hypoxic conditions, as well as HIF1-regulated genes and proteins, in the regulation of ovarian function.
en-copyright=
kn-copyright=

en-aut-name=NishimuraRyo
en-aut-sei=Nishimura
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OkudaKiyoshi
en-aut-sei=Okuda
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Laboratory of Reproductive Endocrinology, Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Laboratory of Reproductive Endocrinology, Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=angiogenesis
kn-keyword=angiogenesis
en-keyword=apoptosis
kn-keyword=apoptosis
en-keyword=corpus luteum
kn-keyword=corpus luteum
en-keyword=follicular development
kn-keyword=follicular development
en-keyword=luteal formation
kn-keyword=luteal formation
en-keyword=luteal regression
kn-keyword=luteal regression
en-keyword=steroidogenesis
kn-keyword=steroidogenesis
END