scholarly journals Real-time dynamics of prostaglandin F2α release from uterus and corpus luteum during spontaneous luteolysis in the cow

Reproduction ◽  
2004 ◽  
Vol 128 (2) ◽  
pp. 189-195 ◽  
Author(s):  
Koumei Shirasuna ◽  
Hitomi Asaoka ◽  
Tomas J Acosta ◽  
Missaka P B Wijayagunawardane ◽  
Masayuki Ohtani ◽  
...  

Prostaglandin (PG) F2α released from the uterus in a pulsatile fashion is essential to induce regression of the corpus luteum (CL) in the cow. In addition to the uterus, the CL has also been recognized as a site of PGF2α production. Therefore, this study aimed to determine the detailed dynamics of the releasing profile of CL-derived PGF2α together with uterus-derived PGF2α during spontaneous luteolysis in the cow. Non-lactating Holstein cows (n = 6) were surgically implanted with a microdialysis system (MDS) on day 15 (oestrus = day 0) of the oestrous cycle. Simultaneously, catheters were implanted to collect ovarian venous plasma ipsilateral to the CL as well as jugular venous plasma. The concentrations of PGF2α, 13,14-dihydro-15-keto-PGF2α (PGFM) and progesterone in the MDS and plasma samples were determined by enzyme immunoassays. The intra-luteal PGF2α secretion slightly increased after the onset of luteolysis (0 h) and drastically increased from 24 h, and was maintained at high levels towards the following oestrus. Furthermore, PGF2α was released from the CL into the ovarian vein in a pulsatile manner during spontaneous luteolysis. Also, the fact that intra-luteal secretion of PGF2α and PGFM showed a positive correlation indicates the existence of a local metabolic pathway for PGF2α in the CL. In conclusion, the present study clarified the real-time dynamics of uterus-derived PGF2α and CL-derived PGF2α during spontaneous luteolysis in the cow, and gives the first in vivo evidence that the CL releases PGF2α during spontaneous luteolysis in the cow. Although the physiological relevance of CL-derived PGF2α appears to be restricted to a local role as an autocrine/paracrine factor in the CL, overall results support the concept that the local release of PGF2α within the regressing CL amplifies the luteolytic action of PGF2α from the uterus.

2010 ◽  
Vol 24 (3) ◽  
pp. 632-643 ◽  
Author(s):  
Edward Arvisais ◽  
Xiaoying Hou ◽  
Todd A. Wyatt ◽  
Koumei Shirasuna ◽  
Heinrich Bollwein ◽  
...  

Abstract Little is known about the early intracellular events that contribute to corpus luteum regression. Experiments were designed to determine the effects of prostaglandin F2α (PGF2α) on phosphatidylinositol-3-kinase (PI3K)/Akt signaling in the corpus luteum in vivo and in vitro. Treatment of midluteal-phase cows with a luteolytic dose of PGF2α resulted in a rapid increase in ERK and mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6K1) signaling and a rapid suppression of Akt phosphorylation in luteal tissue. In vitro treatment of primary cultures of luteal cells with PGF2α also resulted in an increase in ERK and mTOR/p70S6K1 signaling and a diminished capacity of IGF-I to stimulate PI3K, Akt, and protein kinase C ζ activation. Accounting for the reductions in PI3K and Akt activation observed in response to PGF2α treatment, we found that PGF2α promoted the phosphorylation of serine residues (307, 612, 636) in the insulin receptor substrate 1 (IRS1) peptide sequence in vivo and in vitro. Serine phosphorylation of IRS1 was associated with reduced formation of IGF-I-stimulated IRS1/PI3Kp85 complexes. Furthermore, treatment with inhibitors of the MAPK kinase 1/ERK or mTOR/p70S6K1 signaling pathways prevented PGF2α-induced serine phosphorylation of IRS1 and abrogated the inhibitory actions of PGF2α on Akt activation. Taken together, these experiments provide compelling evidence that PGF2α treatment stimulates IRS1 serine phosphorylation, which may contribute to a diminished capacity to respond to IGF-I. It seems likely that the rapid changes in phosphorylation events are among the early events that mediate PGF2α-induced corpus luteum regression.


2010 ◽  
Vol 207 (12) ◽  
pp. 2733-2749 ◽  
Author(s):  
Rachel S. Friedman ◽  
Peter Beemiller ◽  
Caitlin M. Sorensen ◽  
Jordan Jacobelli ◽  
Matthew F. Krummel

The real-time dynamics of the T cell receptor (TCR) reflect antigen detection and T cell signaling, providing valuable insight into the evolving events of the immune response. Despite considerable advances in studying TCR dynamics in simplified systems in vitro, live imaging of subcellular signaling complexes expressed at physiological densities in intact tissues has been challenging. In this study, we generated a transgenic mouse with a TCR fused to green fluorescent protein to provide insight into the early signaling events of the immune response. To enable imaging of TCR dynamics in naive T cells in the lymph node, we enhanced signal detection of the fluorescent TCR fusion protein and used volumetric masking with a second fluorophore to mark the T cells expressing the fluorescent TCR. These in vivo analyses and parallel experiments in vitro show minimal and transient incorporation of TCRs into a stable central supramolecular activating cluster (cSMAC) structure but strong evidence for rapid, antigen-dependent TCR internalization that was not contingent on T cell motility arrest or cSMAC formation. Short-lived antigen-independent TCR clustering was also occasionally observed. These in vivo observations demonstrate that varied TCR trafficking and cell arrest dynamics occur during early T cell activation.


1978 ◽  
Vol 55 (s4) ◽  
pp. 191s-193s ◽  
Author(s):  
Michael J. Dunn

1. Renal venous and urinary prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) were measured in spontaneously hypertensive (SH) rats and Wistar-Kyoto normotensive rats (WKy) of 4 different ages, ranging from 4 to 54 weeks. 2. Renal venous (plasma) PGE2 and PGF2α were similar in WKy and SH rats at all ages, except for greater PGF2α in 40–54 week old SH rats. 3. Urinary (24 h) PGE2 and PGF2α were similar in WKy and SH rats at all ages, except for greater PGE2 in 7–12 week old SH rats. 4. There was a significant trend for renal venous and urinary PGE2 and PGF2α to decrease with advancing age. 5. These experiments did not show evidence that the SH rat kidney, in vivo, has an abnormality of PGE2 or PGF2α production or degradation, which alters secretion or excretion of either prostaglandin.


Author(s):  
Gerben van Hameren ◽  
Graham Campbell ◽  
Marie Deck ◽  
Jade Berthelot ◽  
Benoit Gautier ◽  
...  

Endocrinology ◽  
2003 ◽  
Vol 144 (8) ◽  
pp. 3301-3305 ◽  
Author(s):  
Carlos Stocco ◽  
Jean Djiane ◽  
Geula Gibori

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.


1991 ◽  
Vol 19 (02) ◽  
pp. 163-169 ◽  
Author(s):  
Satoshi Usuki

The effect of Tokishakuyakusan (TS) on the corpus luteum function in pseudopregnant rats was examined in vivo. On day 4 of pseudopregnancy (PSP), induced by cervical stimulation, TS (20 μg) stimulated the progesterone secretion rate (PSR) in the ovarian venous plasma. There was also a significant increase in the rate of progesterone to 20 α-OH-progesterone. However, on day 8 of PSP, there was no apparent change in PSR in the ovarian venous plasma after the administration of TS. These data suggest that the sensitivity to TS of the corpus luteum varies according to its age.


2022 ◽  
Author(s):  
Alice C Yuen ◽  
Anadika R Prasad ◽  
Vilaiwan M Fernandes ◽  
Marc Amoyel

Extracellular Signal-Regulated Kinase (ERK) lies downstream of a core signalling cascade that controls all aspects of development and adult homeostasis. Recent developments have led to new tools to image and manipulate the pathway. However, visualising ERK activity in vivo with high temporal resolution remains a challenge in Drosophila. We adapted a kinase translocation reporter (KTR) for use in Drosophila, which shuttles out of the nucleus when phosphorylated by ERK. We show that ERK-KTR faithfully reports endogenous ERK signalling activity in developing and adult tissues, and that it responds to genetic perturbations upstream of ERK. Using ERK-KTR in time-lapse imaging, we made two novel observations: firstly, sustained hyperactivation of ERK by expression of dominant-active Epidermal Growth Factor Receptor raised the overall level but did not alter the kinetics of ERK activity; secondly, heterogeneity in ERK activity in retinal basal glia correlated with the direction of migration of individual cells. Our results show that KTR technology can be applied in Drosophila to monitor ERK activity in real-time and suggest that this modular tool can be further adapted to study other kinases.


Endocrinology ◽  
2011 ◽  
Vol 152 (7) ◽  
pp. 2797-2805 ◽  
Author(s):  
Wenxiang Luo ◽  
Francisco J. Diaz ◽  
Milo C. Wiltbank

This study tested the hypotheses that prostaglandin (PG) F2α increases expression of genes related to recruitment of leukocytes in mature but not early corpus luteum (CL) and that insensitivity to PGF2α action in early CL is dependent on high intraluteal progesterone (P4) concentrations. Experiment 1 examined early (0.5 h) and late (10 h) in vivo effects of PGF2α on mature (d 17 of pseudopregnancy) and early (d 9) porcine CL. Real-time PCR was used to measure mRNA for chemokines (IL8, CXCL2, CCL2, CCL8, CCL4, CCL11) and chemokine receptors (CCR1, CCR2, CXCR2, CCR5). Western blotting was used to measure protein expression and phosphorylation of nuclear factor-κB proteins. Treatment with PGF2α for 10 h increased mRNA for almost all of these genes (all expect CXCL2 and CCL11) in d 17 CL but not d 9 CL. Treatment with PGF2α also led to greater phosphorylation of nuclear factor-κB-1A protein in d 17 than d 9 CL. Experiment 2 had a 2 × 2 factorial design with d 9 gilts treated or not treated with epostane (3β-hydroxysteroid dehydrogenase inhibitor to suppress intraluteal P4) and treated or not treated with PGF2α. Treatment with PGF2α (10 h) or epostane alone did not induce expression of any of these genes in d 9 CL. However, PGF2α + epostane increased expression of all of these genes except CCL11. In conclusion, PGF2α increases mRNA for chemokines and chemokine receptors in mature CL with similar PGF2α effects induced in early CL if intraluteal P4 is suppressed prior to PGF2α treatment.


1990 ◽  
Vol 42 (5-6) ◽  
pp. 792-800 ◽  
Author(s):  
Jan Olofsson ◽  
Ensio Norjavaara ◽  
Gunnar Selstam

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