scholarly journals Fbxw8 Is Essential for Cul1-Cul7 Complex Formation and for Placental Development

2006 ◽  
Vol 26 (16) ◽  
pp. 6157-6169 ◽  
Author(s):  
Ryosuke Tsunematsu ◽  
Masaaki Nishiyama ◽  
Shuhei Kotoshiba ◽  
Toru Saiga ◽  
Takumi Kamura ◽  
...  
Keyword(s):  
Complex Formation ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Abnormal Development ◽  
Placental Development ◽  
Intrauterine Growth ◽  
Independent Functions ◽  
Vessel Structure ◽  
Heterodimeric Complex ◽  
F Box Protein

ABSTRACT Cullin-based ubiquitin ligases (E3s) constitute one of the largest E3 families. Fbxw8 (also known as Fbw6 or Fbx29) is an F-box protein that is assembled with Cul7 in an SCF-like E3 complex. Here we show that Cul7 forms a heterodimeric complex with Cul1 in a manner dependent on Fbxw8. We generated mice deficient in Fbxw8 and found that Cul7 did not associate with Cul1 in cells of these mice. Two-thirds of Fbxw8 −/− embryos die in utero, whereas the remaining one-third are born alive and grow to adulthood. Fbxw8 −/− embryos show intrauterine growth retardation and abnormal development of the placenta, characterized by both a reduced thickness of the spongiotrophoblast layer and abnormal vessel structure in the labyrinth layer. Although the placental phenotype of Fbxw8 −/− mice resembles that of Cul7 −/− mice, other abnormalities of Cul7 −/− mice are not apparent in Fbxw8 −/− mice. These results suggest that the Cul7-based SCF-like E3 complex has both Fbxw8-dependent and Fbxw8-independent functions.

scholarly journals Fetal Programming Is Deeply Related to Maternal Selenium Status and Oxidative Balance; Experimental Offspring Health Repercussions

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 2085
Author(s):  
María Luisa Ojeda ◽  
Fátima Nogales ◽  
Inés Romero-Herrera ◽  
Olimpia Carreras
Keyword(s):  
Oxidative Stress ◽  
Growth Retardation ◽  
Fetal Programming ◽  
Intrauterine Growth Retardation ◽  
Antioxidant Properties ◽  
Experimental Studies ◽  
Abnormal Development ◽  
Endocrine Regulation ◽  
Intrauterine Growth ◽  
Oxidative Balance

Nutrients consumed by mothers during pregnancy and lactation can exert permanent effects upon infant developing tissues, which could represent an important risk factor for diseases during adulthood. One of the important nutrients that contributes to regulating the cell cycle and tissue development and functionality is the trace element selenium (Se). Maternal Se requirements increase during gestation and lactation. Se performs its biological action by forming part of 25 selenoproteins, most of which have antioxidant properties, such as glutathione peroxidases (GPxs) and selenoprotein P (SELENOP). These are also related to endocrine regulation, appetite, growth and energy homeostasis. In experimental studies, it has been found that low dietary maternal Se supply leads to an important oxidative disruption in dams and in their progeny. This oxidative stress deeply affects gestational parameters, and leads to intrauterine growth retardation and abnormal development of tissues, which is related to endocrine metabolic imbalance. Childhood pathologies related to oxidative stress during pregnancy and/or lactation, leading to metabolic programing disorders like fetal alcohol spectrum disorders (FASD), have been associated with a low maternal Se status and intrauterine growth retardation. In this context, Se supplementation therapy to alcoholic dams avoids growth retardation, hepatic oxidation and improves gestational and breastfeeding parameters in FASD pups. This review is focused on the important role that Se plays during intrauterine and breastfeeding development, in order to highlight it as a marker and/or a nutritional strategy to avoid diverse fetal programming disorders related to oxidative stress.

Molecular approach to intrauterine growth retardation: an overview of recent data

1995 ◽  
Vol 7 (6) ◽  
pp. 1457 ◽  
Author(s):  
E Alsat ◽  
C Marcotty ◽  
R Gabriel ◽  
A Igout ◽  
F Frankenne ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Molecular Mechanisms ◽  
Late Gestation ◽  
Placental Development ◽  
Intrauterine Growth ◽  
Placental Growth Hormone

Consideration of the abnormal regulation of fetal growth leading to intrauterine growth retardation must take account of the fundamental differences between the regulation of growth before and after birth. The significance of endocrine regulators of growth differs greatly in utero. During the first trimester of pregnancy, embryonic growth might be controlled at the level of the individual organs by nutrient supply and by locally active growth factors. Later, fetal growth depends essentially upon materno-placental cooperation in delivering nutrients to the fetus. Therefore the major role of hormones in fetal growth is to mediate utilization of available substrate. Fetal growth seems to be regulated by fetal insulin, IGF-1 and certainly IGF-2, while growth hormone has only a secondary role to play. In late gestation, placental size and fetal growth rate are well correlated, pointing to a key role of the placenta in the regulation of fetal growth. It is therefore of importance to understand the molecular mechanisms involved in regulating placental development and endocrine functions. TGF alpha and EGF might play a major role as suggested by the modulation of their receptors with placental development, and by the specific alterations of epidermal growth factor receptors in intrauterine growth retardation. In addition, human placenta secretes specifically placental growth hormone. The concentration of placental growth hormone is significantly decreased in sera of pregnant women bearing a fetus with intrauterine growth retardation.

Imbalance in the system L-arginin-NO in pathogenesis of obstetric complications and intrauterine growth retardation (Literature review)

2016 ◽  
pp. 43-47
Author(s):  
O.V. Basystyi ◽  
Keyword(s):  
Nitric Oxide ◽  
Literature Review ◽  
Growth Retardation ◽  
Intrauterine Growth Retardation ◽  
Obstetric Complications ◽  
Pathogenetic Role ◽  
Intrauterine Growth ◽  
System L ◽  
Nitric Oxide Deficiency

The data of domestic and foreign literature on etiology, pathogenesis and intrauterine growth retardation diagnosis are presented in the paper. It highlights pathogenetic role of nitric oxide deficiency in case of obstetric complications and intrauterine growth retardation. Key words: intrauterine growth retardation (IUGR), system L-arginin–NO, obstetric complications.

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