Disease relevance of Luteolysis

• Patterns of follicular growth in cows under-going heat stress were associated with decreased serum estradiol from d 11 to 21 and on the day of luteolysis [1].
• Prostaglandin F2alpha induced luteolysis, hypothermia, and abortions in beagle bitches [2].
• A classical acute phase response, as assessed by SAA, was observed during the expulsive stage, but not during luteolysis [3].
• PRL-induced structural luteolysis in the experimental group (hyperprolactinemic) was assessed by the structural characteristics and by the CL weight loss on day 22 in comparison with that exhibited by control rats [4].
• Iproniazid, a very specific monoamine oxidase inhibitor, at a dose level of 200 mg/kg body weight induced luteolysis and caused lysis of deciduomata as well as resorption of the established embryos [5].

Psychiatry related information on Luteolysis

• As PGF2alpha directly stimulated Ang II release, Ang II may influence the critical period for starting the cascade of functional luteolysis in vivo and might lead to structural luteolysis with ET-1 as a major vasoconstrictor [6].

High impact information on Luteolysis

• In many nonprimate mammalian species, cyclical regression of the corpus luteum (luteolysis) is caused by the episodic pulsatile secretion of uterine PGF2alpha, which acts either locally on the corpus luteum by a countercurrent mechanism or, in some species, via the systemic circulation [7].
• Regardless of the mechanism, intraovarian luteolysis in primates (progesterone withdrawal) appears to be the primary stimulus for the subsequent production of endometrial prostaglandins associated with menstruation [7].
• Neither the timing nor the severity of PMS symptoms was altered by mifepristone-induced menses or luteolysis [8].
• Mechanisms controlling corpus luteum function in sheep, cows, nonhuman primates, and women especially in relation to the time of luteolysis [9].
• Induction of luteolysis in the human with a long-acting analog of luteinizing hormone-releasing factor [10].

Chemical compound and disease context of Luteolysis

• In cattle, endometrial expression of integrin alphavbeta3 is reduced on day 16 of the estrous cycle, coinciding with the critical period during which the decision is made to initiate luteolysis or continue with pregnancy [11].

Biological context of Luteolysis

• Because key ovarian functions, such as ovulation and luteolysis, represent aseptic inflammatory responses, and because the theca cell is the functional equivalent of the Leydig cell, we explored the CRH presence in the ovary, first, by specific CRH immunohistochemistry of adult cycling female Sprague-Dawley rat ovaries [12].
• COX-1-deficient mice demonstrated impaired luteolysis, as evidenced by elevated serum progesterone concentration and ovarian histology late in gestation, and delayed induction of uterine oxytocin receptors [13].
• The separation of signaling pathways that govern differentiation and survival in the ovary thereby provides a mechanism by which progesterone production, which is absolutely essential for the maintenance of pregnancy, can continue despite the cessation of proliferation of luteal cells and their commitment to cell death (luteolysis) [14].
• Despite high P and E(2) concentrations during the early luteal phase in all three groups, luteolysis started prematurely, presumably because of excessive negative steroid feedback resulting in suppressed pituitary LH release [15].
• We suggest that gap junctional communication between the cells of the primate and human corpus luteum may be important in hormone synthesis and secretion and may be involved in the process of luteolysis through luteal cell apoptosis [16].

Anatomical context of Luteolysis

• In conclusion, our results suggest that both gonadotropins (FSH and hCG) and cytokines (TGFbeta1 and M-CSF) may be involved in the support of luteal function via suppression of apoptosis, and that TNFalpha and PGF2alpha may contribute to ovarian dysfunction and/or luteal regression via its induction in human luteinized granulosa cells [17].
• In addition, CRH is secreted by the human placenta, rat Leydig cells, and rat and human ovaries, where it may participate in the inflammatory processes of ovulation and luteolysis, and/or the regulation of steroidogenesis [18].
• Lipid accumulation is a hallmark of corpus luteum regression and we characterized lipids stored in rat corpora lutea of pregnancy between days 21 and 24 post coitum, the period of luteolysis [19].
• The infusion of recombinant bovine interferon-alpha I 1 into the uterus of cyclic cows from day 15.5 to 21 after estrus delayed luteolysis [20].
• Development of antral follicles in cattle after prostaglandin-induced luteolysis: changes in serum hormones, steroids in follicular fluid, and gonadotropin receptors [21].

Associations of Luteolysis with chemical compounds

• Whether such amplification of episodic PGF2alpha pulses by luteal oxytocin is a necessary requirement for luteolysis in ruminants remains to be determined [7].
• The results of these studies indicate that the administration of alloxan before the onset of PSP effectively inhibits luteal function, whereas D-1A treatment induces early luteolysis as compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)[22]
• These studies have demonstrated a synergism of estrogen and CB-154 in the induction of luteolysis in cynomolgus monkeys [23].
• Hydrogen peroxide (H2O2), notably released by activated leukocytes, is generated in the rat corpus luteum at luteolysis and evokes luteolytic-like effects in rat luteal cells [24].
• Concentrations of GnRH receptor mRNA increased 2-fold during luteolysis and were higher than control values 12 h after PGF2 alpha treatment (P < 0.05) [25].

Gene context of Luteolysis

• In contrast, simultaneous oxytocin and COX-1 deficiency restored the normal onset of labor by allowing luteolysis in the absence of elevated PGF2alpha production [13].
• The purpose of the present study was to examine the effects on IGFBP-3 production of prostaglandin (PG)-E2, a compound known to stimulate luteal function and prevent/delay luteal regression (a luteotropic compound), and PGF2 alpha, a compound known to be luteolytic [26].
• Dynamic changes in mitogen-activated protein kinase (MAPK) activities in the corpus luteum of the bonnet monkey (Macaca radiata) during development, induced luteolysis, and simulated early pregnancy: a role for p38 MAPK in the regulation of luteal function [27].
• These results suggest that COX-1-derived PGs are responsible for the induction of luteolysis, and that COX-2-derived PGs play a role in the final pathway of parturition [28].
• Thus, the aims of this investigation were to examine whether IL-6 plays a role in luteolysis and, more specifically, to determine whether luteal cells express the IL-6 gene, whether this expression is developmentally and hormonally regulated in pregnancy, and whether the corpus luteum could be a target for IL-6 action [29].

Analytical, diagnostic and therapeutic context of Luteolysis

• The relation between the effects of hysterectomy, decidual tissue, prolactin, or luteinizing hormone (LH) and the ability of indomethacin to prevent luteolysis in rats bearing LH-dependent corpora lutea [30].
• Hypophysectomy on day 10, however, induced rapid, uninterrupted and permanent luteolysis in all rats (15); this was not affected by indomethacin (7 rats) or LHAS (8 rats) [30].
• Radioactively labeled microspheres were used to measure luteal blood flow in pseudopregnant rabbits in which estrogen had been withdrawn to initiate premature luteal regression and in pseudopregnant rabbits injected with hCG [31].
• Densitometric intensities of the electrophoresed IFN-gamma PCR products revealed a drop in RNA expression during late diestrus and at one hour of prostaglandin-induced luteolysis (P < 0.05) [32].
• Lack of evidence from radioimmunoassay for a surge of relaxin secretion into the systemic circulation prior to luteolysis in the pig estrous cycle suggests that the relaxin localized in the luteal cells of the cycle may have an intraovarian function [33].

References