Oncostatin M is produced during pregnancy by decidual cells and stimulates the release of HCG

Ogata, Isao; Shimoya, Koichiro; Moriyama, Akihiro; Shiki, Yasuhiko; Matsumura, Yoshiaki; Yamanaka, Kazuo; Nobunaga, Toshikatsu; Tokugawa, Yoshihiro; Kimura, Tadashi; Koyama, Masayasu; Azuma, Chihiro; Murata, Yuji

doi:10.1093/molehr/6.8.750

Cited by 28 publications

(29 citation statements)

References 21 publications

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“…The action of Stat3 during decidualization may be mediated by IL-11. In addition, oncostatin M produced by decidual cells can stimulate the release of human chorionic gonadotropin (hCG) in humans (Ogata et al 2000), while hCG is essential for the luteal rescue during the maternal recognition of pregnancy (Duncan 2000). Therefore, how oncostatin M acts during decidualization remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Signal transducer and activator of transcription 3 (Stat3) expression and activation in rat uterus during early pregnancy

Teng

Diao²,

Ma³

et al. 2004

Reproduction

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Signal transducer and activator of transcription 3 (Stat3), a member of the Stat family, is specifically activated during mouse embryo implantation. The aim of this study was to investigate the expression, activation and regulation of Stat3 in rat uterus during early pregnancy, pseudopregnancy, delayed implantation and artificial decidualization. Stat3 mRNA was highly expressed in the luminal epithelium on day 5 and in the luminal epithelium and underlying stromal cells at implantation sites on day 6 of pregnancy. There was a strong level of Stat3 protein expression and phosphorylation in the stromal cells near the lumen and in the luminal epithelium on day 5 of pregnancy, which was similar to day 5 of pseudopregnancy. In the afternoon of day 6, the strong level of Stat3 phosphorylation was detected only in the luminal epithelium. Stat3 was highly expressed and activated in the decidual cells from days 7 to 9 of pregnancy and under artificial decidualization in the present study. Our results suggest that the strong level of Stat3 activation in the luminal epithelium and underlying stromal cells during the preimplantation period may be important for establishing uterine receptivity as in mice, and the high level of Stat3 expression and activation in decidual cells may play a role during decidualization.

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Section: Discussionmentioning

confidence: 99%

Signal transducer and activator of transcription 3 (Stat3) expression and activation in rat uterus during early pregnancy

Teng

Diao²,

Ma³

et al. 2004

Reproduction

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“…4). The role of OsM has not been previously investigated in the mouse uterus, but the in human it is reported to reduce proliferation and induce differentiation in uterine stroma in the secretory phase (Ogata et al 2000, Ohata et al 2001) and has been implicated in tissue remodelling in other systems. It has been shown to upregulate both matrix metalloproteinases (MMPs) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) in diverse cell types (Richards et al 1993, Korzus et al 1997, Sanchez et al 2004 as well as tissue plasminogen activator and plasminogen activator inhibitor (Macfelda et al 2002, Spence et al 2002, while in human vascular smooth muscle cells it induces alkaline phosphatase (Shioi et al 2002) and in astocytes Cox-2 (Repovic et al 2003).…”

Section: Stromal Phenotype In the Presence Or Absence Of Lifmentioning

confidence: 99%

Leukaemia inhibitory factor in implantation and uterine biology

Kimber¹

2005

Reproduction

147

110

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Leukaemia inhibitory factor (LIF) is one of the most important cytokines in the reproductive tract. Without expression of LIF in the uterus, implantation of a blastocyst cannot begin. Yet, 13 years after publication of the phenotype of the LIF knockout mouse we are only just beginning to understand how LIF functions in the uterus. This review addresses our knowledge of the role of LIF in regulating implantation through its influence on the luminal epithelium and stromal decidualization, but also its influence on reproductive tract cells such as leukocytes and glandular epithelium, during the pre-implantation phase of pregnancy.Reproduction (

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“…Little is known about the effects of OSM on pregnancy, although OSM concentrations in the sera of pregnant women were found to be significantly higher than that in the sera of non-pregnant women, throughout the pregnancy period [7,8]. It is possible that OSM may affect the invasion and migration processes of the EVTs through various mechanisms, including its effect on EMT during early pregnancy.…”

Section: Introductionmentioning

confidence: 99%

Oncostatin M stimulates cell migration and proliferation by down-regulating E-cadherin in HTR8/SVneo cell line through STAT3 activation

Choi

Kang

et al. 2013

Reprod Biol Endocrinol

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BackgroundDuring the first trimester of pregnancy, trophoblastic E-cadherin expression is down-regulated, thereby allowing extravillous trophoblasts (EVTs) to acquire the potential for migration and invasiveness. The aim of the present study was to investigate the role of OSM on the migration and proliferation of EVT cell line HTR8/SVneo with regard to its effects on the expression of E-cadherin and STAT3 activation.MethodsWe investigated the effects of OSM on RNA and protein expression of E-cadherin by real time RT-PCR analyses, western blotting, and indirect immunofluorescence staining in HTR8/SVneo cells, as well as the effects on cell migration and proliferation. The selective signal transducer and activator of transcription (STAT)3 inhibitor, stattic, and STAT3 siRNA were used to investigate STAT3 activation by OSM.ResultsOSM significantly reduced RNA and protein expression of E-cadherin. Indirect immunofluorescence staining of HTR8/SVneo cells also revealed the down-regulation of E-cadherin, compared with the controls. OSM-stimulated cell migration was attenuated by anti-gp130 antibodies. OSM-induced STAT3 phosphorylation, and the down-regulation of E-cadherin by OSM treatment was restored by stattic and STAT3 siRNA. In addition, OSM-stimulated migration and proliferation were significantly suppressed by STAT3 inhibition.ConclusionsThis study suggests that OSM stimulates the migration and proliferation of EVTs during the first trimester of pregnancy through the down-regulation of E-cadherin. In addition, this study suggests that the effects of OSM on migration and proliferation are related to STAT3 activation, which is important in trophoblast invasiveness.

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Oncostatin M is produced during pregnancy by decidual cells and stimulates the release of HCG

Cited by 28 publications

References 21 publications

Signal transducer and activator of transcription 3 (Stat3) expression and activation in rat uterus during early pregnancy

Signal transducer and activator of transcription 3 (Stat3) expression and activation in rat uterus during early pregnancy

Leukaemia inhibitory factor in implantation and uterine biology

Oncostatin M stimulates cell migration and proliferation by down-regulating E-cadherin in HTR8/SVneo cell line through STAT3 activation

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