scholarly journals Apoptosis During Spontaneous and Prostaglandin F2α-Induced Luteal Regression in the Buffalo Cow (Bubalus bubalis): Involvementof Mitogen-Activated Protein Kinases1

2002 ◽  
Vol 67 (3) ◽  
pp. 752-759 ◽  
Author(s):  
Vijay K. Yadav ◽  
Ranga R. Sudhagar ◽  
R. Medhamurthy
2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Gen Kuroyanagi ◽  
Go Sakai ◽  
Takanobu Otsuka ◽  
Naohiro Yamamoto ◽  
Kazuhiko Fujita ◽  
...  

Abstract Background Heat shock protein 22 (HSP22) belongs to class I of the small HSP family that displays ubiquitous expression in osteoblasts. We previously demonstrated that prostaglandin F2α (PGF2α), a potent bone remodeling factor, induces the synthesis of interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) via p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase in osteoblast-like MC3T3-E1 cells. In the present study, we investigated whether HSP22 is implicated in the PGF2α-induced synthesis of IL-6 and VEGF and the mechanism of MC3T3-E1 cells. Methods MC3T3-E1 cells were transfected with HSP22-siRNA. IL-6 and VEGF release was assessed by ELISA. Phosphorylation of p44/p42 MAP kinase and p38 MAP kinase was detected by Western blotting. Results The PGF2α-induced release of IL-6 in HSP22 knockdown cells was significantly suppressed compared with that in the control cells. HSP22 knockdown also reduced the VEGF release by PGF2α. Phosphorylation of p44/p42 MAP kinase and p38 MAP kinase was attenuated by HSP22 downregulation. Conclusions Our results strongly suggest that HSP22 acts as a positive regulator in the PGF2α-induced synthesis of IL-6 and VEGF in osteoblasts.


Endocrinology ◽  
1997 ◽  
Vol 138 (8) ◽  
pp. 3103-3111 ◽  
Author(s):  
Masahide Ohmichi ◽  
Koji Koike ◽  
Akiko Kimura ◽  
Kanji Masuhara ◽  
Hiromasa Ikegami ◽  
...  

Abstract In this study, prostaglandin (PG) F2α was found to activate mitogen-activated protein (MAP) kinase and MAP kinase kinase (MEK) in cultured rat puerperal uterine myometrial cells. PGF2α stimulation also led to an increase in phosphorylation of raf-1, son of sevenless (SOS), and Shc. Furthermore, we examined the mechanism by which PGF2α induced MAP kinase phosphorylation. Both pertussis toxin (10 ng/ml), which inactivates Gi/Go proteins, and expression of a peptide derived from the carboxyl terminus of the β-adrenergic receptor kinase 1 (βARK1), which specifically blocks signaling mediated by the βγ subunits of G proteins, blocked the PGF2α-induced activation of MAP kinase. Ritodrine (1 μm), which is known to relax uterine muscle contraction, attenuated PGF2α-induced tyrosine phosphorylation of MAP kinase. Moreover, to examine the role of MAP kinase pathway in uterine contraction, an inhibitor of MEK activity, PD098059, was used. Although MEK inhibitor had no effect on PGF2α-induced calcium mobilization, this inhibitor partially inhibited PGF2α-induced uterine contraction. These results provide evidence that PGF2α stimulates the MAP kinase signaling pathway in cultured rat puerperal uterine myometrial cells through Gβγ protein, suggesting that this new pathway may play an important role in the biological action of PGF2α on these cells.


2022 ◽  
Vol 54 (01) ◽  
pp. 42-49
Author(s):  
Tomoyuki Hioki ◽  
Gen Kuroyanagi ◽  
Kazuhiko Fujita ◽  
Go Sakai ◽  
Tetsu Kawabata ◽  
...  

AbstractIncretins including glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), which are secreted from the small intestine after oral food ingestion, are currently well-known to stimulate insulin secretion from pancreatic β-cells and used for the treatment of type 2 diabetes mellitus. We have previously reported that prostaglandin F2α (PGF2α) stimulates the synthesis of interleukin-6 (IL-6) and osteoprotegerin in osteoblast-like MC3T3-E1 cells, and that IL-6 and osteoprotegerin release are mediated through the p44/p42 mitogen-activated protein (MAP) kinase, p38 MAP kinase or stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) pathways. In the present study, we investigated the effects of incretins including GLP-1 and GIP, on the PGF2α-induced synthesis of IL-6 and osteoprotegerin and examined the detailed mechanism in osteoblast-like MC3T3-E1 cells. We found that GIP and GLP-1 significantly stimulated the PGF2α-induced synthesis of IL-6 in osteoblast-like MC3T3-E1 cells. In addition, GIP and GLP-1 significantly enhanced the PGF2α-induced mRNA expression levels of IL-6. On the other hand, GIP and GLP-1 markedly stimulated the PGF2α-induced synthesis of osteoprotegerin. However, the phosphorylation of p44/p42 MAP kinase, p38 MAP kinase, or JNK induced by PGF2α was not affected by GIP or GLP-1. Therefore, these results strongly suggest that incretins enhance the PGF2α-induced synthesis of IL-6 and osteoprotegerin in osteoblast-like MC3T3-E1 cells. However, these syntheses are not mediated through p44/p42 MAP kinase, p38 MAP kinase, or JNK pathways.


1996 ◽  
Vol 54 (2) ◽  
pp. 347-354 ◽  
Author(s):  
David R.J. Bainbridge ◽  
Morag G. Hunter ◽  
Dennis G. Chapple ◽  
Anthony P.F. Flint ◽  
Henry N. Jabbour

2020 ◽  
Vol 29 (5) ◽  
pp. 1021-1021
Author(s):  
Ahmed Essam Elweza ◽  
Enas Abd El-aziz Tahoun ◽  
Ibrahim Said Abu-Alya ◽  
Hamed Talaat Elbaz

2008 ◽  
Vol 291 (1-2) ◽  
pp. 27-32 ◽  
Author(s):  
Chiho Minamitani ◽  
Takanobu Otsuka ◽  
Shinji Takai ◽  
Rie Matsushima-Nishiwaki ◽  
Seiji Adachi ◽  
...  

Reproduction ◽  
2009 ◽  
Vol 138 (1) ◽  
pp. 163-175 ◽  
Author(s):  
María E Matzkin ◽  
Silvia I Gonzalez-Calvar ◽  
Artur Mayerhofer ◽  
Ricardo S Calandra ◽  
Mónica B Frungieri

We have previously observed expression of prostaglandin-endoperoxide synthase 2 (PTGS2), the key enzyme in the biosynthesis of prostaglandins (PGs), in reproductively active Syrian hamster Leydig cells, and reported an inhibitory role of PGF2α on hamster testicular steroidogenesis. In this study, we further investigated PTGS2 expression in hamster Leydig cells during sexual development and photoperiodic gonadal regression. Since PTGS2 is mostly expressed in pubertal and reproductively active adult hamsters with high circulating levels of LH and androgens, we studied the role of these hormones in the regulation/maintenance of testicular PTGS2/PGF2α. In active hamster Leydig cells, LH/hCG and testosterone induced PTGS2 and PGF2α production, and their actions were abolished by the antiandrogen bicalutamide (Bi). These results indicate that LH does not exert a direct effect on PG synthesis. Testosterone also stimulated phosphorylation of the mitogen-activated protein kinase isoforms 3/1 (MAPK3/1) within minutes and hours, but the testosterone metabolite dihydrotestosterone had no effect on PTGS2 and MAPK3/1. Because Bi and U0126, an inhibitor of the MAP kinase kinases 1 and 2 (MAP2K1/2), abolished testosterone actions on MAPK3/1 and PTGS2, our studies suggest that testosterone directly induces PTGS2/PGF2α in hamster Leydig cells via androgen receptors and a non-classical mechanism that involves MAPK3/1 activation. Since PGF2α inhibits testosterone production, it might imply the existence of a regulatory loop that is setting a brake on steroidogenesis. Thus, the androgen environment might be crucial for the regulation of testicular PG production at least during sexual development and photoperiodic variations in hamsters.


1976 ◽  
Vol 68 (3) ◽  
pp. 445-451 ◽  
Author(s):  
F. R. BLATCHLEY ◽  
B. T. DONOVAN ◽  
N. L. POYSER

SUMMARY The presence of beads in the guinea-pig uterus caused premature regression of the corpora lutea, and a corresponding decrease in utero-ovarian venous plasma levels of progesterone, by days 9–10 of the oestrous cycle. If the beads were placed in one horn only, premature luteal regression occurred only in the adjacent ovary. Induced luteal regression was preceded by an increased release of prostaglandin F2α (PGF2α) from the uterine horns which contained the beads. Oestradiol benzoate treatment of guinea-pigs carrying beads in one uterine horn overcame the unilateral effect and resulted in premature luteal regression in both ovaries. This was also associated with the early release of PGF2α from both uterine horns, though a difference in the timing of the release was apparent between the bead-containing (experimental) and control horns.


1976 ◽  
Vol 69 (2) ◽  
pp. 275-286 ◽  
Author(s):  
D. T. BAIRD ◽  
R. B. LAND ◽  
R. J. SCARAMUZZI ◽  
A. G. WHEELER

SUMMARY The concentrations of oestradiol, androstenedione, progesterone and prostaglandin F2α (PGF2α) were measured in utero-ovarian venous blood collected throughout six oestrous cycles in two ewes with utero-ovarian autotransplants. The secretion of oestradiol was closely correlated with that of androstenedione (r = 0·67, P < 0·001) indicating a common origin from the Graafian follicle. The concentration of these two steroids fluctuated at random throughout the luteal phase with the maximum secretion occurring about 2 days before the onset of oestrus. Functional regression of the corpus luteum, as indicated by a fall in the secretion of progesterone, began on day 12 or day 13, i.e. about 4 days before the onset of oestrus. In five of the six cycles the first significant rise in the secretion of PGF2α occurred on days 12–14 at the time of decline of progesterone secretion, although the release of PGF2α was maximal on the day before the onset of oestrus. There was very little release of PGF2α from the uterus before day 12. The temporal relationship of these events suggests that the uterus will only release PGF2α after it has been primed for 7–10 days with progesterone. The initiation of luteal regression is independent of secretion of oestradiol by the pre-ovulatory follicle which may, however, stimulate the further release of PGF2α responsible for irreversible structural luteolysis on the day of pro-oestrus.


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