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

Peluffo, M; Bussmann, Leonardo E.; Stouffer, Richard L.; Tesone, Marta

doi:10.1530/rep.1.00910

Cited by 21 publications

(24 citation statements)

References 55 publications

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“…A study in pregnant Sprague-Dawley rats showed an increase in the activity of caspases 2, 8 and 9 that corresponded to the peak concentration of progesterone in the pregnant females, resulting in an increase in the number of apoptotic cells in the ovary (23). Our assumption is in accordance with these results, in terms of the increase in apoptotic cells in the presence of progesterone.…”

Section: -------------------------------------------------supporting

confidence: 88%

Effect of estradiol, progesterone and testosterone on apoptosis- and proliferation-induced MAPK signaling in human umbilical vein endothelial cells

Powazniak¹

2009

Mol Med Rep

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Abstract. Sex hormones induce death or cell proliferation in various cell lines and in primary cultures. However, the signal transduction pathways involved in the regulation of proliferation and apoptosis in endothelial cells have not been fully elucidated. Here, we report that progesterone and testosterone induce apoptosis in HUVECs in a p38-and JNK-dependent manner, and that estradiol promotes proliferation via the activation of ERK2. We showed that, at physiological doses, progesterone and testosterone promoted p38, but not JNK, phosphorylation. Hormone inhibitors, on the other hand, prevented p38 phosphorylation. When supraphysiological doses were applied, both p38 and JNK were phosphorylated, causing apoptotic cell death. The addition of hormone inhibitors at an appropriate concentration did not prevent cell death or the phosphorylation of p38 and JNK. Estradiol, at physiological doses, promoted an increase in ERK2 phosphorylation that was blocked by fulvestrant. At physiological and supraphysiological doses, it promoted a proliferative effect. In conclusion, these findings suggest that JNK has an important pro-apoptotic function following progesterone and testosterone treatment in human endothelial cells, and that ERK2 has a proliferative effect following estradiol treatment.

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Section: -------------------------------------------------supporting

confidence: 88%

Effect of estradiol, progesterone and testosterone on apoptosis- and proliferation-induced MAPK signaling in human umbilical vein endothelial cells

Powazniak¹

2009

Mol Med Rep

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“…Moreover, depending on the balance between pro-and antiapoptotic proteins, the initiator CASPASE9 is activated and several effector caspases such as CASPASE3 (CASP3) or CASPASE7 are sequentially activated and promote apoptosis in various systems (Budihardjo et al 1999). In previous studies, we reported the expression and activation of proapoptotic caspase-mediated pathways during both spontaneous luteolysis in pregnancy and natural cycles, and PGF2a-induced luteolysis (Peluffo et al 2006, Hernandez et al 2009). In addition, different reports have demonstrated the interaction between the Notch signaling and PI3K/ AKT pathways in cancer cells (Meurette et al 2009, Wang et al 2011.…”

Section: Introductionmentioning

confidence: 99%

A link between Notch and progesterone maintains the functionality of the rat corpus luteum

et al. 2015

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In this study, we investigated the interaction between the Notch pathway and progesterone to maintain the functionality of the corpus luteum (CL). When Notch signaling is activated, the g-secretase complex releases the active intracellular domains (NICD) of their receptors, which exert survival effects. We designed studies to analyze whether the in vitro inhibition of Notch affects progesterone production, steroidogenic regulators, apoptotic parameters, and signaling transduction pathways in the cultures of CL isolated from pregnant and superovulated rats. We detected a decrease in progesterone production when corpora lutea (CL) were incubated with N-(N-(3,5-difluorophenacetyl-L-alanyl))-S-phenylglycine t-butyl ester (DAPT), a g-secretase inhibitor. This effect could be in part due to the decrease detected in the CL protein levels of P450scc because STAR and 3b-hydroxysteroid dehydrogenase were not affected by Notch inhibition. Besides, the addition of aminoglutethimide to the CL culture medium decreased NICD of NOTCH1. We observed an increase in the expression of active CASPASE3 (CASP3) after inhibition by Notch, which was reversed by the presence of progesterone. The BAX:BCLX L ratio was increased in CL treated with DAPT and the presence of progesterone reversed this effect. In addition, phosphorylation of AKT was inhibited in CL treated with DAPT, but had no effect on ERK activation. To demonstrate that the action of DAPT is specifically related with the inhibition of Notch, CLs were incubated with DLL4 antibody and a decrease in progesterone production was detected. These results suggest the existence of a novel link between progesterone and the Notch signaling pathway to maintain the functionality of the CL.

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“…Its main function, progesterone (P 4 ) production, allows for the maintenance of pregnancy [1]. In the absence of gestation, CL regression, which is characterized by changes and degeneration of both vascular and steroidogenic cells, is essential for normal ovarian cyclicity and resumption of a new estrous cycle [2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Is FAS/Fas Ligand System Involved in Equine Corpus Luteum Functional Regression?1

Galvão¹,

Ramilo²,

Skarzynski³

et al. 2010

Biology of Reproduction

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Proapoptotic factor Fas ligand (FASL) and its cell surface receptor FAS are tumor necrosis factor superfamily members that trigger apoptosis in different cell types. However, their influence on luteal steroidogenesis is not clearly understood. The aim of the present work was to determine (i) the presence of the cytokine FASL and its receptor FAS in the mare's corpus luteum (CL) throughout the luteal phase, as well as (ii) the influence of FASL alone, or together with the cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), on equine luteal cell production of luteotrophic and luteolytic factors, cell viability, and apoptosis. FASL and FAS protein expression and mRNA transcription were evaluated in different luteal stages of the equine CL by Western blotting and real-time PCR assays, respectively. Protein expression and FASL mRNA transcription increased in the late CL. Also, FAS and FASL proteins were present in large steroidogenic and endothelial CL cells throughout the luteal phase, as demonstrated by immunohistochemistry. Equine luteal cells isolated from midluteal phase CL were stimulated without (control) or with exogenous cytokines: FASL (10 ng/ml); TNF+IFNG (10 ng/ml each; positive control) or FASL+TNF+IFNG (10 ng/ml each). FASL clearly inhibited in vitro progesterone and prostaglandin E(2) (PGE(2)) production by equine luteal cells but increased prostaglandin F(2alpha) (PGF(2alpha)). Furthermore, FASL effect on equine luteal cell viability depended on the presence of cytokines TNF and IFNG. In conclusion, this study shows the presence of FASL and FAS in the equine CL and suggests their importance in functional luteolysis.

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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

Cited by 21 publications

References 55 publications

Effect of estradiol, progesterone and testosterone on apoptosis- and proliferation-induced MAPK signaling in human umbilical vein endothelial cells

Effect of estradiol, progesterone and testosterone on apoptosis- and proliferation-induced MAPK signaling in human umbilical vein endothelial cells

A link between Notch and progesterone maintains the functionality of the rat corpus luteum

Is FAS/Fas Ligand System Involved in Equine Corpus Luteum Functional Regression?1

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