Apoptosis Induced by Antigestagen RU486 in Rat Corpus Luteum of Pregnancy

Telleria, Carlos; Goyeneche, Alicia A.; Cavicchia, Juan C.; Stati, Arturo O.; Deis, R. P.

doi:10.1385/endo:15:2:147

Cited by 45 publications

(37 citation statements)

References 41 publications

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“…Apoptosis of the luteal cells has been examined during spontaneous and induced CL regression in several animal species, [6][7][8][9][10][11][12] and the death receptor-and mitochondria-mediated apoptotic pathways are involved in the apoptosis of luteal cells. 13,15 A previous study suggested that hormonal-induced pseudopregnant rat ovaries were used as the model for regression of the CL, and a pseudopregnant CL could only be maintained for a certain number of days, after which spontaneous regression occurs.…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic Reticulum Stress-Mediated Apoptotic Pathway Is Involved in Corpus Luteum Regression in Rats

et al. 2015

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Endoplasmic reticulum stress (ERS), which is a novel pathway of regulating cellular apoptosis and the function of ERS during corpus luteum (CL) regression, is explored. Early-luteal stage (day 2), mid-luteal stage (day 7), and late-luteal stage (day 14 and 20) were induced, and the apoptosis of luteal cells was detected by a terminal 2 0 -deoxyuridine 5 0 -triphosphate nick-end labeling (TUNEL) assay. The apoptotic cells were increased with the regression of CL, especially during the late-luteal stage. The ERS markers glucose-regulated protein 78 (Grp78), CCAAT/enhancer-binding protein homologous protein (CHOP), X-box binding protein 1 (XBP1), activating transcription factor 6a (ATF6a), eukaryotic initiation factor 2a (eIF2a), inositol-requiring protein 1a (IRE1a), caspase 12, and apoptosis marker caspase 3 were analyzed by real-time polymerase chain reaction (PCR) and immunohistochemistry, in agreement with the results of the TUNEL assay; the expression levels of CHOP, caspase 12, and caspase 3 were increased during the process of CL regression. Luteal cells were isolated and cultured in vitro, and the apoptosis of luteal cells was induced by prostaglandin F2a. The ERS was attenuated by the ERS inhibitor tauroursodeoxycholic acid, and the apoptotic rate was analyzed by flow cytometry. The ERS markers Grp78, CHOP, XBP1s, ATF6a, eIF2a, IRE1a, caspase 12, and apoptotic execute marker caspase 3 were analyzed by real-time PCR and immunofluorescence, and the results suggested that the expression of CHOP, caspase 12, and caspase 3 were increased, and there was increased apoptosis of luteal cells. But the expression of IRE1a/XBP1s and eIF2a was not detected. Taken together, the ERS is involved in the CL regression of rats through the CHOP and caspase 12 pathway.

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Section: Discussionmentioning

confidence: 99%

Endoplasmic Reticulum Stress-Mediated Apoptotic Pathway Is Involved in Corpus Luteum Regression in Rats

et al. 2015

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“…5B), as luteolysis progressed. Moreover, CL sections stained with hematoxylineosin were used to count apoptotic cells at estrus and DII stages following a validated morphologic procedure (Telleria et al 2001), considering only luteal cells with advanced signs of apoptosis (i.e., containing multiple nuclear fragments or small densely stained nucleus). Similar results were obtained using this procedure (data not shown), as compared to the TUNEL assay.…”

Section: Tunelmentioning

confidence: 99%

Expression of caspase-2, -3, -8 and -9 proteins and enzyme activity in the corpus luteum of the rat at different stages during the natural estrous cycle

Peluffo¹,

Bussmann²,

Stouffer³

et al. 2006

Reproduction

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Apoptosis is associated with the regression of the corpus luteum (CL) in many species. Since caspases play a central role in apoptosis, we studied several initiators (-2, -8, and -9) and the main effector (-3) caspase in the CL during the estrous cycle of the rat. Two different populations of CL (old and new) were identified on ovaries at estrus and diestrus II (DII). Diminished (P!0.05) luteal progesterone content and P450scc levels suggested that functional luteolysis occurred between the new CL at DII and old CL at estrus, whereas the decline (P!0.05) in luteal weight indicated that structural regression was occurring between old CL at estrus to DII. Immunostaining for caspase-2 in luteal and endothelial cells appeared to increase as the luteal phase progressed, peaking at DII in the old CL. However, caspase-8 and -9 immunostaining showed little change with a slight increase at estrus in the old population. Notably, caspase-3 staining appeared to peak at DII in the new CL. Enzyme activity of caspase-9 increased (P!0.05) in the new CL at DII, followed by that of caspase-2 and -3 in old CL at estrus. Caspase-8 activity did not change at any stage. The number of apoptotic cells increased at DII in the old CL. These results suggest an important role for this protease family during early events of luteolysis in the rat estrous cycle. Reproduction (2006) 132 465-475

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“…Functional luteolysis in rats is associated with morphologic features (26). Thus, the morphology of the CL reflects its capacity to synthesize and secrete P. Because the administration of EGF increased P, we wanted to discern whether the treatment with EGF could affect the number of cells from each population within the CL (26).…”

Section: Resultsmentioning

confidence: 99%

“…The ability of the luteal cells to synthesize and secrete P is intimately associated with the CL functionality (26). CL structure and morphology reflects its functional state.…”

Section: Discussionmentioning

confidence: 99%

Epidermal growth factor prevents prepartum luteolysis in the rat

Ribeiro¹,

Aisemberg²,

Billi³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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We have previously reported that intrauterine (i͞u) administration of epidermal growth factor (EGF 500 ng) on day (d) 21 of pregnancy delayed 19.0 ؎ 0.6 h the onset of labor. Progesterone (P) is secreted by ovarian corpora lutea (CL) throughout gestation in the rat. Prepartum CL regression due to increased uterine cyclooxygenase I and prostaglandin F 2␣ results in P withdrawal followed by labor. The aims of the present work were (i) to study whether EGF delayed-onset of labor was mediated by a mechanism that prevented CL regression; (ii) to determine amniotic fluid (AF) EGF in pregnant rats. Rats on d21 of pregnancy received i͞u EGF (500 ng) and were killed 0, 4, 8, 12, 24, and 48 h later. Control AF from rats on d13 and 18 -22 of pregnancy was obtained. EGF decreased uterine prostaglandin F 2␣ synthesis 8 h after treatment. Twelve hours after EGF injection, P reached its highest serum level and uterine cyclooxygenase I expression was undetectable. CL from rats killed 8 and 12 h after EGF were similar to those from rats on d13 of pregnancy, when serum P is maximum. EGF in AF increased throughout gestation, reached a maximum on d21, and decreased before the onset of labor. We suggest that the effect of EGF on the onset of labor was mediated by an early effect on the uterus that prevented prepartum CL regression.

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Apoptosis Induced by Antigestagen RU486 in Rat Corpus Luteum of Pregnancy

Cited by 45 publications

References 41 publications

Endoplasmic Reticulum Stress-Mediated Apoptotic Pathway Is Involved in Corpus Luteum Regression in Rats

Endoplasmic Reticulum Stress-Mediated Apoptotic Pathway Is Involved in Corpus Luteum Regression in Rats

Expression of caspase-2, -3, -8 and -9 proteins and enzyme activity in the corpus luteum of the rat at different stages during the natural estrous cycle

Epidermal growth factor prevents prepartum luteolysis in the rat

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