References of "NISOLLE, Michelle"
     in
Bookmark and Share    
Full Text
See detailA novel mutation of the luteinizing hormone/choionic gonadotrophin receptor gene leading to Leydig cell hypoplasia type I
Potorac, Iulia ULg; Rivero-Muller, A; Pintiaux, Axelle ULg et al

in The International Journal of The Romania Society of Endocrinology - Abstract book (2015, June)

Detailed reference viewed: 25 (0 ULg)
See detailPelvic pain and Endometriosis
BRICHANT, Géraldine ULg; NISOLLE, Michelle ULg

Conference (2015, May 08)

Detailed reference viewed: 21 (1 ULg)
Full Text
Peer Reviewed
See detailA novel mutation of the luteinizing hormone/choionic gonadotrophin receptor gene leading to Leydig cell hypoplasia type I
Potorac, Iulia ULg; Rivero-Müller, A; Pintiaux, Axelle ULg et al

in Symposium "Perspectives in Endocrinology" - 5ème édition (2015, February 07)

Detailed reference viewed: 20 (3 ULg)
Full Text
Peer Reviewed
See detailESTETROL AND ITS NEUROPROTECTIVE EFFECT IN NEONATAL HYPOXIC-ISCHEMIC ENCEPHALOPATHY
Tskitishvili, Ekaterine ULg; Nisolle, Michelle ULg; Noël, Agnès ULg et al

in The 12th World Congress of Perinatal Medicine, Madrid, 3-6 November 2015 (2015)

Perinatal hypoxic-ischemic encephalopathy (HIE) occurs in 1-8 cases per live 1000 births. Brain hypoxia and ischemia due to systemic hypoxemia and reduced cerebral blood flow (CBF) are the primary causes ... [more ▼]

Perinatal hypoxic-ischemic encephalopathy (HIE) occurs in 1-8 cases per live 1000 births. Brain hypoxia and ischemia due to systemic hypoxemia and reduced cerebral blood flow (CBF) are the primary causes of neonatal HIE accompanied by gray and white matter injuries occurring in neonates. About 20% of affected newborns die in the postnatal period, and an additional 25% will sustain childhood disabilities. So far no medical treatment provides important neuroprotection against HIE. Studies of new neuroprotective agents in animal models of HIE may provide important information pertinent to the development of treatments for this pathological condition. Estetrol (E4) is a recently described estrogen with four hydroxyl-groups that is synthesized exclusively during pregnancy by the human fetal liver. It has important antioxidative activity. In this study, in vitro we defined antioxidative effect of E4 on primary hippocampal cell cultures, taken from newborn rat pups, before/after induction of oxidative stress. To examine oxidative stress and cell viability, lactate dehydrogenase (LDH) activity and cell survival (MTS) assays were performed on primary neuronal cell cultures. To study the neuroprotective and therapeutic effects of E4 in vivo neonatal HIE model of 7-day-old newborn rat pups was used. Rat pups body temperatures were examined along with their body and brain weights. Brains were studied at the level of the hippocampus and cortex. Intact cell counting and expressions of markers for neuronal cell viability (microtubule-associated protein-2 (MAP-2)), neurogenesis (doublecortin (DCX)) and angiogenesis (vascular-endothelial growth factor (VEGF)) were evaluated by histo- and immunohistochemistry. The serum levels of brain damage markers (S100B and glial fibrillary acidic protein (GFAP)) were measured by ELISA. Our results demonstrate for the first time that E4 has a significant neuroprotective and therapeutic effects. Also, E4 has powerful antioxidative and cell survival properties in vitro. It decreases the early gray matter loss and promotes neuro- and angiogenesis in vivo. Estetrol treatment has no effects on body weight, brain weight or body temperature. Taken together, E4 might become an important safe and physiological substance to treat neonatal HIE. [less ▲]

Detailed reference viewed: 52 (5 ULg)
Full Text
Peer Reviewed
See detailHypoxic-Ischemic Encephalopathy and Premature Babies Brain Damage: Impact of Estetrol
Tskitishvili, Ekaterine ULg; Nisolle, Michelle ULg; Noël, Agnès ULg et al

in The 11th Congress of the European Society of Gynecology, Prague 21-24 October, 2015 (2015)

Neonatal hypoxic-ischemic brain injury remains a main problem of perinatal medicine. About 20% of affected newborns die in the postnatal period, and an additional 25% will sustain childhood disabilities ... [more ▼]

Neonatal hypoxic-ischemic brain injury remains a main problem of perinatal medicine. About 20% of affected newborns die in the postnatal period, and an additional 25% will sustain childhood disabilities mostly in the form of motor and cognitive delays. The nature of the deficits is dependent on the gestational age and severity of the insult, though it is s seldom reported in preterm infants. No medical treatment provides important neuroprotection against HIE. Studies in animal models of HIE may provide important information for the development of treatment for this pathological condition. Estetrol (E4) is a recently described estrogen with four hydroxyl-groups that is synthesized exclusively during pregnancy by the human fetal liver. In this study, we defined the antioxidative effect of E4 in primary hippocampal cell cultures taken from newborn rat pups (in vitro) and evaluated its neuroprotective and therapeutic potency in neonatal HIE model of the immature newborn rat (in vivo). Lactate Dehydrogenase (LDH) and cell survival (MTS) assays were performed on primary neuronal cell cultures. Rat pups body temperatures were examined along with their body and brain weights. Brains were studied at the level of the hippocampus and cortex. Intact cell counting and expressions of markers for neuronal cell viability (microtubule-associated protein-2 (MAP-2)), neurogenesis (doublecortin (DCX)) and angiogenesis (vascular-endothelial growth factor (VEGF)) were evaluated by histo- and immunohistochemistry. The serum levels of two markers of brain damage (S100B and glial fibrillary acidic protein (GFAP)) were measured by ELISA. Our results demonstrate that E4 has a significant neuroprotective and therapeutic dose-dependent effects. Estetrol has powerful antioxidative and cell survival effects in vitro. It decreases the early gray matter loss and promotes neuro- and angiogenesis in vivo. Estetrol treatment has no effects on body weight, brain weight or body temperature. Taken together, Estetrol might become an important safe and physiological substance to treat neonatal HIE. [less ▲]

Detailed reference viewed: 27 (4 ULg)
Full Text
Peer Reviewed
See detailIn vitro evaluation of the anti-apoptotic drug Z-VAD-FMK on human ovarian granulosa cell lines for further use in ovarian tissue transplantation.
Fransolet, Maïté ULg; HENRY, Laurie ULg; Labied, Soraya et al

in Journal of Assisted Reproduction & Genetics (2015)

PURPOSE: Because ovarian granulosa cells are essential for oocyte survival, we examined three human granulosa cell lines as models to evaluate the ability of the pan-caspase inhibitor benzyloxycarbonyl ... [more ▼]

PURPOSE: Because ovarian granulosa cells are essential for oocyte survival, we examined three human granulosa cell lines as models to evaluate the ability of the pan-caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (Z-VAD-FMK) to prevent primordial follicle loss after ovarian tissue transplantation. METHODS: To validate the efficacy of Z-VAD-FMK, three human granulosa cell lines (GC1a, HGL5, COV434) were treated for 48 h with etoposide (50 mug/ml) and/or Z-VAD-FMK (50 muM) under normoxic conditions. To mimic the ischemic phase that occurs after ovarian fragment transplantation, cells were cultured without serum under hypoxia (1 % O2) and treated with Z-VAD-FMK. The metabolic activity of the cells was evaluated by WST-1 assay. Cell viability was determined by FACS analyses. The expression of apoptosis-related molecules was assessed by RT-qPCR and Western blot analyses. RESULTS: Our assessment of metabolic activity and FACS analyses in the normoxic experiments indicate that Z-VAD-FMK protects granulosa cells from etoposide-induced cell death. When cells are exposed to hypoxia and serum starvation, their metabolic activity is reduced. However, Z-VAD-FMK does not provide a protective effect. In the hypoxic experiments, the number of viable cells was not modulated, and we did not observe any modifications in the expressions of apoptosis-related molecules (p53, Bax, Bcl-xl, and poly (ADP-ribose) polymerase (PARP)). CONCLUSION: The death of granulosa cell lines was not induced in our ischemic model. Therefore, a protective effect of Z-VAD-FMK in vitro for further use in ovarian tissue transplantation could not be directly confirmed. It will be of interest to potentially use Z-VAD-FMK in vivo in xenograft models. [less ▲]

Detailed reference viewed: 36 (3 ULg)
Full Text
Peer Reviewed
See detailA novel inactivating mutation of the LH/chorionic gonadotrophin receptor with impaired membrane trafficking leading to Leydig cell hypoplasia type 1.
Rivero-Muller, Adolfo; Potorac, Iulia ULg; Pintiaux, Axelle ULg et al

in European journal of endocrinology / European Federation of Endocrine Societies (2015), 172(6), 27-36

OBJECTIVE: The LH/chorionic gonadotrophin receptor (LHCGR) is a G protein-coupled receptor (GPCR) that plays a central role in male sexual differentiation, regulation of ovarian follicular maturation ... [more ▼]

OBJECTIVE: The LH/chorionic gonadotrophin receptor (LHCGR) is a G protein-coupled receptor (GPCR) that plays a central role in male sexual differentiation, regulation of ovarian follicular maturation, ovulation and maintenance of corpus luteum and pregnancy, as well as maintenance of testicular testosterone production. Mutations in the LHCGR gene are very rare. The aim of this work was to study the clinical and molecular characteristics of a rare familial LHCGR mutation. METHODS: Five affected members of a family, including a phenotypically female, but genotypically male (46,XY), patient with Leydig cell hypoplasia type 1 and four genotypically female siblings with reproductive abnormalities, were studied genetically. Cell trafficking studies as well as signalling studies of mutated receptor were performed. RESULTS: The five affected patients were all homozygous for a novel mutation in the LHCGR gene, a deletion of guanine in position 1850 (1850delG). This resulted in a frameshift affecting most of the C-terminal intracellular domain. In vitro studies demonstrated that the 1850delG receptor was completely incapable of transit to the cell membrane, becoming trapped within the endoplasmic reticulum. This could not be rescued by small-molecule agonist treatment or stimulated intracellularly by co-expression of a yoked human chorionic gonadotrophin. CONCLUSIONS: This novel LHCGR mutation leads to complete inactivation of the LHCGR receptor due to trafficking and signalling abnormalities, which improves our understanding of the impact of the affected structural domain on receptor trafficking and function. [less ▲]

Detailed reference viewed: 15 (4 ULg)
Full Text
Peer Reviewed
See detailInfluence of mouse strain on ovarian tissue recovery after engraftment with angiogenic factor.
Fransolet, Maïté ULg; Henry, Laurie ULg; Labied, Soraya et al

in Journal of Ovarian Research (2015), 8(1), 14

BACKGROUND: For women facing gonadotoxic treatment, cryopreservation of ovarian tissue with subsequent retransplantation during remission is a promising technique for fertility preservation. However ... [more ▼]

BACKGROUND: For women facing gonadotoxic treatment, cryopreservation of ovarian tissue with subsequent retransplantation during remission is a promising technique for fertility preservation. However, follicle loss within grafted ovarian tissue can be caused by ischemia and progressive revascularization. Several xenograft models using different immunodeficient rodent lines are suitable for studying ovarian tissue survival and follicular viability after frozen-thawed ovarian cortex transplantation. SCID mice, which are deficient for functional B and T cells, are the most commonly used mice for ovarian xenograft studies. However, due to incomplete immunosuppression, NOD-SCID mice displaying low NK cell function and an absence of circulating complement might be more appropriate. The present study aims to define the most appropriate immunodeficient mouse strain for ovarian tissue xenotransplantation by comparing ovarian graft recovery in SCID and NOD-SCID mice following engraftment in the presence of isoform 111 of vascular endothelial growth factor. METHODS: Sheep ovarian cortex fragments were embedded in a collagen matrix, with or without VEGF111, before being stitched onto the ovaries of SCID and NOD-SCID mice. Transplants were recovered after 3 days to study early revascularization or after 3 weeks to evaluate follicle preservation and tissue fibrosis through histological analyses. RESULTS: At day 3, vessels were largely reorganized in the ovarian grafts of both mouse strains. After 3 weeks, the cortical tissue was clearly identifiable in SCID mice but not in NOD-SCID mice. Upon VEGF111 treatment, vascularization was significantly improved 3 days after transplantation in SCID mice. This increase in vessel density was correlated with better follicular preservation in SCID mice 3 weeks after transplantation. Fibrosis was not decreased by VEGF treatment in either mouse strain. CONCLUSIONS: Tissue architecture and follicular morphology were better preserved in ovarian tissues grafted in SCID mice in comparison with NOD-SCID mice. Moreover, tissue revascularization was improved in SCID mice by VEGF111 graft treatment. Thus, we consider SCID mice to be the best murine model for studying ovarian tissue xenografts. [less ▲]

Detailed reference viewed: 22 (3 ULg)