Prenatal exposure to nicotine impairs protective responses of rat pups to hypoxia in an age-dependent manner

2001 ◽  
Vol 127 (1) ◽  
pp. 61-73 ◽  
Author(s):  
James E Fewell ◽  
Francine G Smith ◽  
Vienna K.Y Ng
Keyword(s):  
Prenatal Exposure ◽  
Dependent Manner ◽  
Rat Pups ◽  
Age Dependent

Second-trimester maternal lipid profiles predict pregnancy complications in an age-dependent manner

2019 ◽  
Vol 299 (5) ◽  
pp. 1253-1260 ◽  
Author(s):  
Qi Wu ◽  
Lixia Zhang ◽  
Licong Huang ◽  
Yu Lei ◽  
Lin Chen ◽  
...  
Keyword(s):  
Pregnancy Complications ◽  
Lipid Profiles ◽  
Dependent Manner ◽  
Second Trimester ◽  
Age Dependent

Deletion of murine tau gene increases tau aggregation in a human mutant tau transgenic mouse model

2010 ◽  
Vol 38 (4) ◽  
pp. 1001-1005 ◽  
Author(s):  
Kunie Ando ◽  
Karelle Leroy ◽  
Céline Heraud ◽  
Anna Kabova ◽  
Zehra Yilmaz ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Double Mutant ◽  
Transgenic Mouse Model ◽  
Tau Proteins ◽  
Dependent Manner ◽  
Age Dependent ◽  
Ad Alzheimer’S Disease ◽  
Tau Aggregation ◽  
The Brain

We have reported previously a tau transgenic mouse model (Tg30tau) overexpressing human 4R1N double-mutant tau (P301S and G272V) and that develops AD (Alzheimer's disease)-like NFTs (neurofibrillary tangles) in an age-dependent manner. Since murine tau might interfere with the toxic effects of human mutant tau, we set out to analyse the phenotype of our Tg30tau model in the absence of endogenous murine tau with the aim to reproduce more faithfully a model of human tauopathy. By crossing the Tg30tau line with TauKO (tau-knockout) mice, we have obtained a new mouse line called Tg30×TauKO that expresses only exogenous human double-mutant 4R1N tau. Whereas Tg30×TauKO mice express fewer tau proteins compared with Tg30tau, they exhibit augmented sarkosyl-insoluble tau in the brain and an increased number of Gallyas-positive NFTs in the hippocampus. Taken together, exclusion of murine tau causes accelerated tau aggregation during aging of this mutant tau transgenic model.

scholarly journals Random errors in protein synthesis activate an age-dependent program of muscle atrophy in mice

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
James Moore ◽  
Rashid Akbergenov ◽  
Martina Nigri ◽  
Patricia Isnard-Petit ◽  
Amandine Grimm ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Muscle Atrophy ◽  
Strength Analysis ◽  
Dependent Manner ◽  
Random Errors ◽  
Age Related ◽  
Related Phenotype ◽  
Age Dependent ◽  
Translation Accuracy ◽  
Transcriptomic Changes

AbstractRandom errors in protein synthesis are prevalent and ubiquitous, yet their effect on organismal health has remained enigmatic for over five decades. Here, we studied whether mice carrying the ribosomal ambiguity (ram) mutation Rps2-A226Y, recently shown to increase the inborn error rate of mammalian translation, if at all viable, present any specific, possibly aging-related, phenotype. We introduced Rps2-A226Y using a Cre/loxP strategy. Resulting transgenic mice were mosaic and showed a muscle-related phenotype with reduced grip strength. Analysis of gene expression in skeletal muscle using RNA-Seq revealed transcriptomic changes occurring in an age-dependent manner, involving an interplay of PGC1α, FOXO3, mTOR, and glucocorticoids as key signaling pathways, and finally resulting in activation of a muscle atrophy program. Our results highlight the relevance of translation accuracy, and show how disturbances thereof may contribute to age-related pathologies.

TRPV1 deletion exacerbates hyperthermic seizures in an age-dependent manner in mice

2016 ◽  
Vol 128 ◽  
pp. 27-34 ◽  
Author(s):  
Karlene T. Barrett ◽  
Richard J.A. Wilson ◽  
Morris H. Scantlebury
Keyword(s):  
Dependent Manner ◽  
Age Dependent

Loss of miR-83 extends lifespan and affects target gene expression in an age-dependent manner in Caenorhabditis elegans

2018 ◽  
Vol 45 (12) ◽  
pp. 651-662 ◽  
Author(s):  
Emmanuel Enoch Dzakah ◽  
Ahmed Waqas ◽  
Shuai Wei ◽  
Bin Yu ◽  
Xiaolin Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Target Gene ◽  
Dependent Manner ◽  
Target Gene Expression ◽  
Age Dependent

Methylation of the ESR1 CpG island in the colorectal mucosa is an ‘all or nothing’ process in healthy human colon, and is accelerated by dietary folate supplementation in the mouse

2005 ◽  
Vol 33 (4) ◽  
pp. 709-711 ◽  
Author(s):  
N.J. Belshaw ◽  
G.O. Elliott ◽  
E.A. Williams ◽  
J.C. Mathers ◽  
L. Buckley ◽  
...  
Keyword(s):  
Cpg Island ◽  
Cancer Cell Line ◽  
Human Colon ◽  
Colorectal Cancer Cell Line ◽  
Dependent Manner ◽  
Folate Supplementation ◽  
Healthy Human ◽  
Dietary Folate ◽  
Human Dna ◽  
Age Dependent

ESR1 is frequently silenced by CGI (CpG island) methylation, both in human colorectal tumours and, in an age-dependent manner, in healthy mucosa. It is not clear, however, whether methylation of individual cytosines occurs randomly within the epithelial genome, or preferentially within individual cells as an ‘all-or-nothing’ phenomenon. CGI methylation can be quantified in human DNA residues recovered from faecal samples. We used bisulphite genomic sequencing of human DNA from this source and from a colorectal cancer cell line (SW48) to show that the ESR1 CGI is methylated in an allele-specific manner. This provides support for the ‘all or none’ mechanism for methylation of this gene, and shows how age-dependent methylation of the ESR1 CGI leads rapidly to silencing of the gene within the cells, and hence the colonic crypt within which it occurs. Preliminary studies with a rodent model suggest the rate of age-dependent methylation of ESR1 is modifiable by dietary folate.

Fetal alcohol spectrum disorder (FASD) affects the hippocampal levels of histone variant H2A.Z-2

2019 ◽  
Vol 97 (4) ◽  
pp. 431-436 ◽  
Author(s):  
Taylor L. Gretzinger ◽  
Monica Tyagi ◽  
Christine J. Fontaine ◽  
Manjinder S. Cheema ◽  
María González-Perez ◽  
...  
Keyword(s):  
Prenatal Exposure ◽  
Fetal Alcohol Spectrum Disorder ◽  
Critical Role ◽  
Transcriptional Regulators ◽  
Histone Variant ◽  
Spectrum Disorder ◽  
Fetal Alcohol ◽  
Rat Pups ◽  
Epigenetic Patterns ◽  
Fetal Alcohol Spectrum

Fetal alcohol spectrum disorder (FASD) is caused by prenatal exposure to ethanol and has been linked to neurodevelopmental impairments. Alcohol has the potential to alter some of the epigenetic components that play a critical role during development. Previous studies have provided evidence that prenatal exposure to ethanol results in abnormal epigenetic patterns (i.e., hypomethylation) of the genome. The aim of this study was to determine how prenatal exposure to ethanol in rats affects the hippocampal levels of expression of two important brain epigenetic transcriptional regulators involved in synaptic plasticity and memory consolidation: methyl CpG-binding protein 2 (MeCP2) and histone variant H2A.Z. Unexpectedly, under the conditions used in this work we were not able to detect any changes in MeCP2. Interestingly, however, we observed a significant decrease in H2A.Z, accompanied by its chromatin redistribution in both female and male FASD rat pups. Moreover, the data from reverse-transcription qPCR later confirmed that this decrease in H2A.Z is mainly due to down-regulation of its H2A.Z-2 isoform gene expression. Altogether, these data provide strong evidence that prenatal exposure to ethanol alters histone variant H2A.Z during neurogenesis of rat hippocampus.

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