Laboratory of Reproductive Biology

Marseille, France

Laboratory of Reproductive Biology

Marseille, France
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Rolland L.,Obstetrics and Reproductive Medicine | Rolland L.,CNRS Mediterranean Institute for Biodiversity and Ecology Marine and Continental | Courbiere B.,Obstetrics and Reproductive Medicine | Courbiere B.,CNRS Mediterranean Institute for Biodiversity and Ecology Marine and Continental | And 8 more authors.
Toxicology in Vitro | Year: 2017

Our objective was to optimize the CA technique on mammal embryos. Materials and methods 1000 frozen 2-cell embryos from B6CBA mice were used. Based on a literature review, and after checking post-thaw embryo viability, the main outcome measures included: 1) comparison of the embryo recovery rate between 2 CA protocols (2 agarose layers and 3 agarose layers); 2) comparison of DNA damage by the CA on embryos with (ZP +) and without (ZP −) zona pellucida; and 3) comparison of DNA damage in embryos exposed to 2 genotoxic agents (H2O2 and simulated sunlight irradiation (SSI)). DNA damage was quantified by the % tail DNA. Results 1) The recovery rate was 3,3% (n = 5/150) with the 2 agarose layers protocol and 71,3% (n = 266/371) with the 3 agarose layers protocol. 2) DNA damage did not differ statistically significantly between ZP − and ZP + embryos (12.60 ± 2.53% Tail DNA vs 11.04 ± 1.50 (p = 0.583) for the control group and 49.23 ± 4.16 vs 41.13 ± 4.31 (p = 0.182) for the H2O2 group); 3) H2O2 and SSI induced a statistically significant increase in DNA damage compared with the control group (41.13 ± 4.31% Tail DNA, 36.33 ± 3.02 and 11.04 ± 1.50 (p < 0.0001)). The CA on mammal embryos was optimized by using thawed embryos, by avoiding ZP removal and by the adjunction of a third agarose layer. © 2017 Elsevier Ltd


Ruiz-Sanchez E.,Instituto Nacional Of Neurologia Y Neurocirugia | Yescas P.,Instituto Nacional Of Neurologia Y Neurocirugia | Rodriguez-Violante M.,Instituto Nacional Of Neurologia Y Neurocirugia | Martinez-Rodriguez N.,Hospital Infantil Of Mexico | And 8 more authors.
Journal of the Neurological Sciences | Year: 2017

Introduction The NR4A2 transcription factor is important in the development, survival and phenotype of dopaminergic neurons and it is postulated as a possible biomarker for Parkinson's disease (PD). Therefore, our aim was to analyze in a sample of a Mexican population with idiopathic PD, mutations (in two hotspot mutation regions) and two polymorphisms (rs34884856 in promotor and rs35479735 intronic regions) of the NR4A2 gene. We also evaluate the levels of NR4A2 gene expression in peripheral blood for a Mexican population, and identify whether they are associated with NR4A2 gene polymorphisms. Methods We conducted a case-control study, which included 227 idiopathic PD cases and 454 unrelated controls. Genetic variants of the NR4A2 gene were genotyped by high-resolution melting (HRM) and validated by an automated sequencing method. The gene expression was performed in peripheral blood using a real-time polymerase chain reaction. Results The rs35479735 polymorphism was associated with a higher risk of developing PD. In addition, NR4A2 gene expression was significantly decreased in patients with PD. Linkage disequilibrium analysis showed a haplotype H4 (3C-3G) that showed lower levels of expression, and contained the risk alleles for both polymorphisms. Conclusions In summary, this is the first study in a Mexican population that considers the analysis of NR4A2 in patients with PD. An association was identified between genotype and mRNA expression levels of NR4A2 in patients with PD. These results suggest that polymorphisms and expression of the NR4A2 gene could play an important role in the risk of developing PD in Mexican populations. © 2017 Elsevier B.V.


Vaiman D.,French Institute of Health and Medical Research | Vaiman D.,University of Paris Descartes | Gascoin-Lachambre G.,French Institute of Health and Medical Research | Gascoin-Lachambre G.,University of Paris Descartes | And 21 more authors.
PLoS ONE | Year: 2011

A low-protein diet applied during pregnancy in the rat results in intrauterine growth restricted (IUGR) fetuses. In humans, IUGR is associated with increased perinatal morbidity, higher incidence of neuro-developmental defects and increased risk of adult metabolic anomalies, such as diabetes and cardiovascular disease. Development and function of many organs are affected by environmental conditions such as those inducing fetal and early postnatal growth restriction. This phenomenon, termed "fetal programming" has been studied unconnectedly in some organs, but very few studies (if any) have investigated at the same time several organs, on a more comparative basis. However, it is quite probable that IUGR affects differentially most organ systems, with possible persistent changes in gene expression. In this study we address transcriptional alterations induced by IUGR in a multi-organ perspective, by systematic analysis of 20-days rat fetuses. We show that (1) expressional alterations are apparently stronger in organs functioning late in foetal or postnatal life than in organs that are functioning early (2) hierarchical classification of the deregulations put together kidney and placenta in one cluster, liver, lungs and heart in another; (3) the epigenetic machinery is set up especially in the placenta, while its alterations are rather mild in other organs; (4) the genes appear deregulated in chromosome clusters; (5) the altered expression cascades varies from organ to organ, with noticeably a very significant modification of the complement and coagulation cascades in the kidney; (6) we found a significant increase in TF binding site for HNF4 proteins specifically for liver genes that are down-regulated in IUGR, suggesting that this decrease is achieved through the action of HNF transcription factors, that are themselves transcriptionnally induced in the liver by IUGR (x 1.84 fold). Altogether, our study suggests that a combination of tissue-specific mechanisms contributes to bring about tissue-driven modifications of gene cascades. The question of these cascades being activated to adapt the organ to harsh environmental condition, or as an endpoint consequence is still raised. © 2011 Vaiman et al.

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