Arginase Inhibition Improves Endothelial Function in an Age-Dependent Manner in Healthy Elderly Humans

2019 ◽  
Vol 22 (5) ◽  
pp. 385-389 ◽  
Author(s):  
Ali Mahdi ◽  
John Pernow ◽  
Oskar Kövamees
2019 ◽  
Vol 299 (5) ◽  
pp. 1253-1260 ◽  
Author(s):  
Qi Wu ◽  
Lixia Zhang ◽  
Licong Huang ◽  
Yu Lei ◽  
Lin Chen ◽  
...  

2010 ◽  
Vol 38 (4) ◽  
pp. 1001-1005 ◽  
Author(s):  
Kunie Ando ◽  
Karelle Leroy ◽  
Céline Heraud ◽  
Anna Kabova ◽  
Zehra Yilmaz ◽  
...  

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.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
James Moore ◽  
Rashid Akbergenov ◽  
Martina Nigri ◽  
Patricia Isnard-Petit ◽  
Amandine Grimm ◽  
...  

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.


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

2018 ◽  
Vol 45 (12) ◽  
pp. 651-662 ◽  
Author(s):  
Emmanuel Enoch Dzakah ◽  
Ahmed Waqas ◽  
Shuai Wei ◽  
Bin Yu ◽  
Xiaolin Wang ◽  
...  

2005 ◽  
Vol 33 (4) ◽  
pp. 709-711 ◽  
Author(s):  
N.J. Belshaw ◽  
G.O. Elliott ◽  
E.A. Williams ◽  
J.C. Mathers ◽  
L. Buckley ◽  
...  

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.


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