scholarly journals Defective Extraembryonic Angiogenesis in Mice Lacking LBP-1a, a Member of the grainyhead Family of Transcription Factors

2004 ◽  
Vol 24 (16) ◽  
pp. 7113-7129 ◽  
Author(s):  
Vishwas Parekh ◽  
Amy McEwen ◽  
Virginia Barbour ◽  
Yutaka Takahashi ◽  
Jerold E. Rehg ◽  
...  
Keyword(s):  
Intrauterine Growth Retardation ◽  
Critical Role ◽  
Binding Motif ◽  
Structural Genes ◽  
Wild Type ◽  
Transcription Factor Family ◽  
Differentiation Markers ◽  
Trophoblast Differentiation ◽  
Intrauterine Growth ◽  
Normal Placenta

ABSTRACT LBP-1a and CP2 are ubiquitously expressed members of the grainyhead transcription factor family, sharing significant sequence homology, a common DNA binding motif, and modulating a range of key regulatory and structural genes. We have reported previously that CP2-null mice are viable with no obvious abnormality. LBP-1a provides redundant function in this context. We show here that mice lacking LBP-1a expression develop intrauterine growth retardation at embryonic day 10.5, culminating in death 1 day later. No focal intraembryonic cause for this CP2-independent defect is evident. In contrast, a significant reduction in the thickness of the labyrinthine layer of the placenta is observed in LBP-1a−/− animals. However, expression of trophoblast differentiation markers is unperturbed in this context, and complementation studies utilizing tetraploid wild-type cells failed to rescue or ameliorate the LBP-1a−/− phenotype, excluding a primary trophoblast defect. An explanation for these observations is provided by the prominent angiogenic defect observed in the mutant placentas. LBP-1a−/− allantoic blood vessels fail to penetrate deeply and branch into the complex embryonic vasculature characteristic of the normal placenta. Interestingly, a similar defect in angiogenesis is observed in the yolk sac vasculature, primary endothelial cell-lined capillary tubes, although present, failed to connect into a characteristic intricate vascular network. Collectively, these results demonstrate that LBP-1a plays a critical role in the regulation of extraembryonic angiogenesis.

scholarly journals Carboxypeptidase E Independently Changes Microtubule Glutamylation, Dendritic Branching, and Neuronal Migration

ASN NEURO ◽  
2022 ◽  
Vol 14 ◽  
pp. 175909142110627
Author(s):  
Chen Liang ◽  
Damien Carrel ◽  
Nisha K. Singh ◽  
Liam L. Hiester ◽  
Isabelle Fanget ◽  
...  
Keyword(s):  
Cortical Neuron ◽  
Neuronal Migration ◽  
Critical Role ◽  
Cortical Plate ◽  
Binding Motif ◽  
Wild Type ◽  
Dendrite Morphology ◽  
Neuron Migration ◽  
Carboxypeptidase E ◽  
The Impact

Neuronal migration and dendritogenesis are dependent on dynamic changes to the microtubule (MT) network. Among various factors that regulate MT dynamics and stability, post-translational modifications (PTMs) of MTs play a critical role in conferring specificity of regulatory protein binding to MTs. Thus, it is important to understand the regulation of PTMs during brain development as multiple developmental processes are dependent on MTs. In this study, we identified that carboxypeptidase E (CPE) changes tubulin polyglutamylation, a major PTM in the brain, and we examine the impact of CPE-mediated changes to polyglutamylation on cortical neuron migration and dendrite morphology. We show, for the first time, that overexpression of CPE increases the level of polyglutamylated α-tubulin while knockdown decreases the level of polyglutamylation. We also demonstrate that CPE-mediated changes to polyglutamylation are dependent on the CPE zinc-binding motif and that this motif is necessary for CPE action on p150Glued localization. However, overexpression of a CPE mutant that does not increase MT glutamylation mimics the effects of overexpression of wild type CPE on dendrite branching. Furthermore, although overexpression of wild type CPE does not alter cortical neuron migration, overexpression of the mutant may act in a dominant-negative manner as it decreases the number of neurons that reach the cortical plate (CP), as we previously reported for CPE knockdown. Overall, our data suggest that CPE changes MT glutamylation and redistribution of p150Glued and that this function of CPE is independent of its role in shaping dendrite development but plays a partial role in regulating cortical neuron migration.

Coronavirus diseases and pregnancy: COVID-19,SARS, and MERS

2020 ◽  
pp. 276-289
Author(s):  
Mobina Fathi ◽  
Kimia Vakili ◽  
Niloofar Deravi
Keyword(s):  
Pregnant Women ◽  
Intrauterine Growth Retardation ◽  
Negative Impact ◽  
World Health ◽  
Wuhan City ◽  
Intrauterine Growth ◽  
Exponential Increase ◽  
The World ◽  
Health Organization ◽  
Respiratory Droplets

Around the end of December 2019, a new beta-coronavirus from Wuhan City, Hubei Province, China began to spread rapidly. The new virus, called SARS-CoV-2, which could be transmitted through respiratory droplets, had a range of mild to severe symptoms, from simple cold in some cases to death in others. The disease caused by SARS-CoV-2 was named COVID-19 by WHO and has so far killed more people than SARS and MERS. Following the widespread global outbreak of COVID-19, with more than 132758 confirmed cases and 4955 deaths worldwide, the World Health Organization declared COVID-19 a pandemic disease in January 2020. Earlier studies on viral pneumonia epidemics has shown that pregnant women are at greater risk than others. During pregnancy, the pregnant woman is more prone to infectious diseases. Research on both SARS-CoV and MERS-CoV, which are pathologically similar to SARS-CoV-2, has shown that being infected with these viruses during pregnancy increases the risk of maternal death, stillbirth, intrauterine growth retardation and, preterm delivery. With the exponential increase in cases of COVID-19 throughout the world, there is a need to understand the effects of SARS-CoV-2 on the health of pregnant women, through extrapolation of earlier studies that have been conducted on pregnant women infected with SARS-CoV, and MERS-CoV. There is an urgent need to understand the chance of vertical transmission of SARS-CoV-2 from mother to fetus and the possibility of the virus crossing the placental barrier. Additionally, since some viral diseases and antiviral drugs may have a negative impact on the mother and fetus, in which case, pregnant women need special attention for the prevention, diagnosis, and treatment of COVID-19.

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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