scholarly journals Maximal expression of suppressors of cytokine signaling in the rat ovary occurs in late pregnancy

Reproduction ◽  
2009 ◽  
Vol 138 (3) ◽  
pp. 537-544 ◽  
Author(s):  
Stephen T Anderson ◽  
Naajia N M Isa ◽  
Johanna L Barclay ◽  
Michael J Waters ◽  
Jon D Curlewis
Keyword(s):  
Mrna Expression ◽  
Prolactin Receptor ◽  
Prostaglandin F2α ◽  
Late Pregnancy ◽  
Placental Lactogen ◽  
Cytokine Signaling ◽  
Pregnant Rats ◽  
Protein Levels ◽  
Rat Ovary ◽  
Suppressors Of Cytokine Signaling

Maintenance of the rodent corpus luteum (CL) during pregnancy requires prolactin receptor (PRLR) signal transduction via STAT5. At the end of pregnancy, prostaglandin F2α (PGF2α) induces luteal regression through many mechanisms, including downregulation of PRLR signaling. We have previously shown that a PGF2α analog upregulates suppressors of cytokine signaling (SOCS) proteins in the CL of day 19 pregnant rats leading to reduced STAT5 signaling. Here, we examined endogenous SOCS expression and STAT5 signaling in the rat ovary during normal pregnancy and luteolysis. The mRNA expression of Socs1, Socs2, and Socs3 and related cytokine-inducible SH2-containing protein (Cish) was low in early pregnancy (day 7), but significantly increased at mid-pregnancy (days 10 and 13) associated with increased endogenous tyrosine phosphorylation (TyrP) of STAT5. In support of the notion that these changes are due to increasing placental lactogen levels at this time, we found that treatment with exogenous PRL on day 7 increased TyrP of STAT5 and induced SOCS mRNA expression, except Socs3. After mid-pregnancy, further significant increases in Socs3 and Cish mRNA expression were observed. Such changes in mRNA expression correlated with protein levels, with protein levels of both SOCS3 and CISH being maximal in late pregnancy (days 19–21). In addition, a significant reduction in TyrP of STAT5 was first observed on day 20, with a further substantial decrease on day 21. Therefore, these results are consistent with the hypothesis that increased SOCS expression in the rat ovary during late pregnancy reduces STAT5 signaling, which may be important in PGF2α-induced luteolysis.

scholarly journals Hormonal control of Luteal 20α-Hydroxy steroid dehydrogenase and Δ5-3β-hydroxy steroid dehydrogenase during luteolysis in the pregnant rat

1975 ◽  
Vol 152 (3) ◽  
pp. 433-443 ◽  
Author(s):  
R G Rodway ◽  
N J Kuhn
Keyword(s):  
Prostaglandin F2α ◽  
Late Pregnancy ◽  
Normal Pregnancy ◽  
Hormonal Control ◽  
Placental Lactogen ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Hydroxy Steroid ◽  
Steroid Dehydrogenase

Treatment of pregnant rats with human chorionic gonadotrophin, luteotrophin (luteinizing hormone), luteotrophin-releasing hormone, prostaglandin F2α, aminoglutethimide, or by foetoplacental removal or hysterectomy achieved a common multiple-response pattern, namely increased activity of luteal 20α-hydroxy steroid dehydrogenase with decreased activity of delta5-3β-hydroxy steriod dehydrogenase and release of delta4-3-oxo steroids in vitro. 2. Similar effects of foetoplacental removal are noted in pregnant mice. 3. Gonadotrophin induced lower activities of 20α-hydroxy steroid dehydrogenase, except at the very end of pregnancy, and partly inhibited the induction caused by foetoplacental removal. 4. The results suggest that existence of a placental factor that restrains these changes until the end of normal pregnancy, which is produced in amounts proportional to the number of placentae and is conveyed to the ovary via the blood. 5. This factor was not replaced by prolactin. 6. It is argued that neither placental lactogen nor pituitary luteotrophin participate in the induction of 20α-hydroxy steroid dehydrogenase at late pregnancy in the rat. 7. Aminoglutethimide induced 20α-hydroxy steroid dehydrogenase only in late pregnancy. This was partly reversed by progesterone, wholly reversed by progesterone plus oestrogen, and did not involve the pituitary.

scholarly journals Expression and possible role of fibroblast growth factor family members in porcine antral follicles during final maturation

Reproduction ◽  
2009 ◽  
Vol 138 (1) ◽  
pp. 141-149 ◽  
Author(s):  
Dieter Schams ◽  
Vera Steinberg ◽  
Martin Steffl ◽  
Heinrich H D Meyer ◽  
Bajram Berisha
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Fibroblast Growth Factor ◽  
Family Members ◽  
Prostaglandin F2α ◽  
Fibroblast Growth ◽  
Protein Levels ◽  
Final Maturation ◽  
Theca Interna

The aim of this study was to investigate the possible participation of fibroblast growth factor (FGF) family members (FGF1, FGF2 and FGF7 and their receptors) in porcine follicles (polyovulatory species) under special consideration for FGF2 during final growth. A classification of follicles was done by size and follicular fluid content of oestradiol-17β, progesterone and prostaglandin F2α. The mRNA expression of examined factors was analysed by real-time PCR. The hormone concentration was estimated by enzyme immunoassay, protein characterisation by western blotting and localisation by immunohistochemistry. Follicle tissue separated in theca interna and granulosa cells was extracted and tested for mRNA of FGF1, FGF2, FGF7 and receptors (FGFR1IIIc, FGFRIIIb and FGFR2IIIc). Additionally, the mRNA expression of FSHR, LHR and aromatase cytochrome P450 for further characterisation of follicles was analysed. Significantly, higher FGF2 protein levels were measured in stroma when compared with total follicle or corpus luteum tissue. This result was confirmed by western blot with two strong bands. Immunological localisation of FGF2 only in stroma (fibroblasts) confirms the protein measurements. The results show a clear difference for FGF2 protein expression during final growth of follicles if monovulatory (bovine) and polyovulatory (porcine) species are compared. FGF2 protein in porcine ovary may be (due to localisation and concentration in stroma) important for support of angiogenesis of more follicles (polyovulatory species) and not of a single follicle like in cows.

scholarly journals Streptozotocin-Induced Diabetes Decreases Mammary Gland Lipoprotein Lipase Activity and Messenger Ribonucleic Acid in Pregnant and Nonpregnant Rats

2002 ◽  
Vol 3 (1) ◽  
pp. 61-68
Author(s):  
Laura Blanco-Dolado ◽  
Antonia Martín-Hidalgo ◽  
Emilio Herrera
Keyword(s):  
Mammary Gland ◽  
Mrna Expression ◽  
Lipoprotein Lipase ◽  
Late Pregnancy ◽  
Insulin Deficiency ◽  
Pregnant Rats ◽  
Messenger Ribonucleic Acid ◽  
Mrna Content ◽  
Plasma Insulin Levels ◽  
Streptozotocin Induced Diabetes

Diabetes mellitus is associated with a reduction of lipoprotein lipase (LPL) activity in adipose tissue and development of hypertriglyceridemia. To determine how a condition of severe insulin deficiency affects mammary gland LPL activity and mRNA expression during late pregnancy, streptozotocin (STZ) treated (40 mg/kg) and non-treated (control) virgin and 20 day pregnant rats were studied. In control rats, both LPL activity and mRNA were higher in pregnant than in virgin rats. When compared to control rats, STZ-treated rats, either pregnant or virgin, showed decreased LPL activity and mRNA content. Furthermore, mammary gland LPL activity was linearly correlated with mRNA content, and either variable was linearly correlated with plasma insulin levels. Thus, insulin deficiency impairs the expression of LPL in mammary glands, revealing the role of insulin as a modulator of the enzyme at the mRNA expression level.

scholarly journals Reduced Hypothalamic Vasopressin Secretion Underlies Attenuated Adrenocorticotropin Stress Responses in Pregnant Rats

Endocrinology ◽  
2005 ◽  
Vol 146 (3) ◽  
pp. 1626-1637 ◽  
Author(s):  
Shuaike Ma ◽  
Michael J. Shipston ◽  
David Morilak ◽  
John A. Russell
Keyword(s):  
Mrna Expression ◽  
Anterior Pituitary ◽  
Late Pregnancy ◽  
Secretory Response ◽  
Receptor Expression ◽  
Pituitary Cells ◽  
Pregnant Rats ◽  
V1b Receptor ◽  
Vasopressin Secretion ◽  
In Pregnancy

We sought to explain decreased ACTH secretory responses to stress in pregnant rats by investigating hypothalamic CRH and vasopressin secretion and actions on anterior pituitary corticotrophs. In late pregnancy median eminence, CRH content was reduced (by 12%). Anterior pituitary proopiomelanocortin mRNA expression, measured by in situ hybridization but not radioimmunoassayed ACTH content, was also reduced (by 45% on d 21); CRH receptor (CRHR)1 mRNA expression was unaltered in pregnancy, but V1b receptor mRNA expression was reduced (by 19%). ACTH secretory responses, measured in jugular blood, to CRH (200 ng/kg iv) or vasopressin (1.7 μg/kg, iv) were reduced on d 21 vs. virgins (49% and 44%), but the response to combined CRH and vasopressin injection was intact. Either antalarmin (CRHR1 antagonist; 20 mg/kg ip) or dP(Tyr(Me)2),Arg-NH29)AVP (V1a/b antagonist; 10 μg/kg, iv) pretreatment reduced the ACTH secretory response to forced swimming (90 sec) in virgin rats (by 57% and 40%), but only antalarmin was effective in pregnant rats (53% decrease). In vitro, measuring ACTH secretion from acutely dispersed anterior pituitary cells showed increased corticotroph sensitivity in pregnancy to CRH and to CRH augmentation by vasopressin, attributable to increased intracellular cAMP action. Hence, in late pregnancy, reduced anterior pituitary CRHR1 or V1b receptor expression did not impair corticotroph responses to CRH or vasopressin. Rather, diminished secretagogue secretion in vivo accounts for reduced action of stress levels of exogenous CRH or vasopressin alone; the late pregnancy attenuated ACTH secretory response to swim stress is deduced to be due to reduced vasopressin release by parvocellular paraventricular nuclei neurones.

scholarly journals The effects of the aromatase inhibitor fadrozole hydrochloride on fetuses and uteri in late pregnant rats

2004 ◽  
Vol 180 (2) ◽  
pp. 337-345 ◽  
Author(s):  
H Tamada ◽  
Y Shimizu ◽  
T Inaba ◽  
N Kawate ◽  
T Sawada
Keyword(s):  
Physical Properties ◽  
Aromatase Inhibitor ◽  
Mrna Expression ◽  
Lysyl Oxidase ◽  
Late Pregnancy ◽  
Estrogen Deficiency ◽  
Uterine Tissue ◽  
Pregnant Rats ◽  
Toxicological Effects ◽  
Matrix Metalloproteinase 1

It is well known that progesterone and estrogen are essential hormones for maintaining pregnancy in most mammals. Some specific roles of progesterone for the maintenance of pregnancy have been clarified, but the role of estrogen is not well known. This study examines the effects of the aromatase inhibitor, fadrozole hydrochloride (Fad), on fetuses, uterine physical properties and the mRNA expression of the uterine enzymes that are related to collagen metabolism during late pregnancy in rats. Continuous s.c. infusion with 300 micro g/day Fad from day 14 of pregnancy (day 1=the day of sperm detection) reduced the concentration of plasma estradiol-17beta (E(2)), and did not change that of plasma progesterone, compared with controls. The treatment increased the intrauterine pressure and reduced the size and compliance of the uterine tissue framework. It also caused injuries (hematomata on the extremities) in about one-quarter of fetuses by day 20. The collagen content of the uterine ampullae was not changed by the treatment. Uterine mRNA expressions of matrix metalloproteinase-1 (MMP-1), which degrades collagens, and of lysyl oxidase (LO), which is necessary for the formation of intra- and inter-molecular cross-links of collagen, were examined by quantitative RT-PCR. The treatment with Fad had no effect on the expression of MMP-1 mRNA and increased that of LO mRNA. Daily s.c. injection with 0.2 micro g E(2) restored the changes in uterine physical properties and the mRNA expression of LO caused by the Fad treatment, and prevented fetal injury, indicating that the influences of Fad treatment are due to estrogen deficiency but not to toxicological effects of Fad. These results imply that estrogen deficiency during late pregnancy in rats obstructs development of the uterine tissue framework so as to cause fetal injury. It is possible that an increase in the uterine expression of LO gene may be involved in this obstruction.

Expression of multidrug resistance-associated protein 2 in small intestine from pregnant and postpartum rats

2001 ◽  
Vol 280 (6) ◽  
pp. G1261-G1273 ◽  
Author(s):  
Aldo D. Mottino ◽  
Tim Hoffman ◽  
Lothar Jennes ◽  
Jingsong Cao ◽  
Mary Vore
Keyword(s):  
Small Intestine ◽  
Multidrug Resistance ◽  
Blot Analysis ◽  
Late Pregnancy ◽  
Female Rats ◽  
Intestinal Cell ◽  
Pregnant Rats ◽  
Control Female ◽  
Protein Levels ◽  
Pregnancy And Lactation

We analyzed the expression of multidrug resistance-associated protein 2 (mrp2) in the small intestine of control female rats and in rats during late pregnancy (19–20 days of pregnancy) and lactation (2–4, 10–14, and 21 days after delivery). Western blot analysis was performed on brush-border membranes prepared from different regions of the small intestine. Expression of mrp2 was maximal in the proximal segments for all experimental groups, was preserved in pregnant rats, and increased by 100% in postpartum rats by late lactation with respect to control animals. Northern blot analysis of mrp2 mRNA revealed a positive correlation with protein levels. Transport of S-glutathione-dinitrophenol (DNP-SG) from the intestinal cell to the lumen was analyzed in the everted intestinal sac model. Secretion of DNP-SG was not altered in pregnant rats but increased in lactating animals by late lactation. Intestinal mrp2 mRNA, protein, and transport activity are increased in lactating rats, suggesting that this may represent an adaptive mechanism to minimize the toxicity of dietary xenobiotics in response to increased postpartum food consumption.

Effect of interferon-γ treatment on the expression of interleukin-1β at the maternal - fetal interface of pregnant rats

2007 ◽  
Vol 19 (3) ◽  
pp. 510 ◽  
Author(s):  
Hong-Fei Xia ◽  
Quan-Hong Sun ◽  
Jing-Pian Peng
Keyword(s):  
Late Pregnancy ◽  
Interferon Γ ◽  
Control Group ◽  
Cytokine Network ◽  
Pregnant Rats ◽  
Endometrial Stromal Cells ◽  
Protein Levels ◽  
Decidua Basalis ◽  
Ifn Γ

In the present study, the possible mechanisms by which interferon (IFN)-γ affects pregnancy were investigated using the cytokine network model. The IFN-γ-induced expression of interleukin (IL)-1β was examined using western blotting, immunohistochemistry and immunofluorescence. The results showed that IFN-γ treatment significantly decreased the expression of uterine IL-1β protein during the preimplantation, post-implantation and mid-gestation periods. The expression of IL-1β protein was increased after IFN-γ treatment compared with the control group in late pregnancy. In the placenta, IL-1β protein levels were significantly increased after IFN-γ treatment in early and mid-pregnancy. In late pregnancy, IFN-γ treatment significantly decreased placental IL-1β protein levels. IL-1β was mainly expressed in the myometrium, uterine arteries, decidua basalis, trophospongium of the junctional layer and trophoblastic epithelium of the labyrinthine layers. IL-1β was mainly located in the cytoplasm of in vitro cultured endometrial stromal cells (ESCs). IFN-γ treatment did not affect the distribution of IL-1β, only the expression of IL-1β. The effects of IFN-γ on the proliferation of ESCs were determined using an MTS (a novel tetrazolium compound) assay. IFN-γ treatment inhibited the proliferation of ESCs and decreased the weight of the fetus and placenta. These results indicate that exogenous IFN-γ affects the expression of IL-1β and inhibits ESC proliferation.

scholarly journals Prostaglandin F2α (PGF2α) and Prolactin Signaling: PGF2α-Mediated Inhibition of Prolactin Receptor Expression in the Corpus Luteum

Endocrinology ◽  
2003 ◽  
Vol 144 (8) ◽  
pp. 3301-3305 ◽  
Author(s):  
Carlos Stocco ◽  
Jean Djiane ◽  
Geula Gibori
Keyword(s):  
Corpus Luteum ◽  
Time Course ◽  
Prolactin Receptor ◽  
Prostaglandin F2α ◽  
Receptor Expression ◽  
Luteal Cell ◽  
Pregnant Rats ◽  
Prolactin Signaling ◽  
Stimulation Of

Abstract It is well established that prolactin (PRL) sustains, whereas prostaglandin F2α (PGF2α) curtails, progesterone production by the rodent corpus luteum (CL). We have previously shown that PGF2α inhibits the expression of several luteal genes stimulated by PRL, whereas it stimulates other genes inhibited by this hormone. We have also found that PGF2α stimulation of 20α-hydroxysteroid dehydrogenase (20αHSD), an enzyme that catabolizes progesterone, at the end of pregnancy is accompanied by a dramatic decrease in PRL receptor (PRL-R) expression. These findings, and the fact that the factors that inhibit PRL-R are not known, led us to examine in vivo whether the decline in PRL-R at the end of pregnancy is due to PGF2α and to also find out whether PGF2α opposes PRL action by inhibiting PRL-R expression. Using the PGF2α receptor (PGF2α-R) knockout, we examined whether the absence of the PGF2α-R prevents the decline in the expression of both the short and long forms of the PRL-R in the CL. We found that, in sharp contrast to the wild-type mice, in which both forms of the PRL-R decline to low levels between d 18–20 of pregnancy, expression of these receptors remained elevated in the PGF2α-R null mice. Furthermore, administration of PGF2α to pregnant rats inhibited PRL-R expression. Time-course analysis revealed that PGF2α treatment decreases both isoforms of PRL-R within 1 h of treatment in vivo, whereas its stimulatory effect on 20αHSD expression was further delayed. Similar results were obtained with luteinized granulosa cells in culture. To examine whether the decline in PRL-R is involved/necessary for PGF2α action, cells were transfected with a constitutively active PRL-R. The expression of this receptor did not prevent PGF2α effect on PRL-R or 20αHSD expression. Taken together, these results demonstrate that PGF2α inhibits the expression of the PRL-R and that the decline in both forms of the PRL-R that occurs at the end of pregnancy in the CL is due to PGF2α. The results further suggest that PGF2α-mediated stimulation of 20αHSD is independent from PGF2α inhibition of PRL signaling in luteal cell.

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