In vivo characterization of endothelial cell activation in a transgenic mouse model of Alzheimer’s disease

Angiogenesis ◽  
2006 ◽  
Vol 9 (2) ◽  
pp. 59-65 ◽  
Author(s):  
Caroline Schultheiss ◽  
Birgit Blechert ◽  
Florian C. Gaertner ◽  
Enken Drecoll ◽  
Jan Mueller ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Cell Activation ◽  
Transgenic Mouse Model ◽  
Endothelial Cell Activation ◽  
Model Of Alzheimer’S Disease ◽  
In Vivo Characterization

scholarly journals The cytoplasmic NPM mutant induces myeloproliferation in a transgenic mouse model

Blood ◽  
2010 ◽  
Vol 115 (16) ◽  
pp. 3341-3345 ◽  
Author(s):  
Ke Cheng ◽  
Paolo Sportoletti ◽  
Keisuke Ito ◽  
John G. Clohessy ◽  
Julie Teruya-Feldstein ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Mouse Model ◽  
Transgenic Mice ◽  
Transgenic Mouse ◽  
Myeloid Leukemia ◽  
Gene Mutations ◽  
Transgenic Mouse Model ◽  
Acute Myeloid

Abstract Although NPM1 gene mutations leading to aberrant cytoplasmic expression of nucleophosmin (NPMc+) are the most frequent genetic lesions in acute myeloid leukemia, there is yet no experimental model demonstrating their oncogenicity in vivo. We report the generation and characterization of a transgenic mouse model expressing the most frequent human NPMc+ mutation driven by the myeloid-specific human MRP8 promoter (hMRP8-NPMc+). In parallel, we generated a similar wild-type NPM trans-genic model (hMRP8-NPM). Interestingly, hMRP8-NPMc+ transgenic mice developed myeloproliferation in bone marrow and spleen, whereas nontransgenic littermates and hMRP8-NPM transgenic mice remained disease free. These findings provide the first in vivo evidence indicating that NPMc+ confers a proliferative advantage in the myeloid lineage. No spontaneous acute myeloid leukemia was found in hMPR8-NPMc+ or hMRP8-NPM mice. This model will also aid in the development of therapeutic regimens that specifically target NPMc+.

scholarly journals A Novel Anti-inflammatory D-peptide Halts Disease Phenotype Progression in an ALS Mouse Model

2020 ◽  
Author(s):  
Julia Post ◽  
Vanessa Kogel ◽  
Anja Schaffrath ◽  
Philipp Lohmann ◽  
Nadim Joni Shah ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Mouse Model ◽  
Brain Stem ◽  
Transgenic Mouse ◽  
Cell Activation ◽  
Therapeutic Potential ◽  
Transgenic Mouse Model ◽  
Lumbar Spinal Cord ◽  
Disease Phenotype ◽  
Model Of Alzheimer’S Disease

Abstract Background: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterised by selective neuronal death in brain stem and spinal cord. The cause is unknown, but an increasing evidence has firmly certified that neuroinflammation plays a key role in ALS pathogenesis. Neuroinflammation is a pathological hallmark of several neurodegenerative disorders and has been implicated as driver of disease progression. Here, we describe two treatment studies demonstrating the therapeutic potential of a tandem version of the well-known all-d-peptide RD2 (RD2RD2) in a transgenic mouse model of Alzheimer’s disease (APP/PS1) and in a transgenic mouse model of ALS (SOD1*G93A).Methods:APP/PS1 and SOD1*G93A mice were treated intraperitoneally for four weeks mice with RD2RD2 vs placebo. APP/PS1 brain and plasma samples were histologically and biochemically analysed for inflammatory markers, gliosis and amyloid pathology. SOD1*G93A mice were tested longitudinally during treatment in various behavioural and motor coordination tests. Brain and spinal cord samples were investigated immunohistochemically for gliosis and neurodegeneration.Results: Treatment in APP/PS1 mice revealed significant reduction in glial cell activation in the brain and significantly lower levels of inflammatory cytokines in plasma. RD2RD2 treatment in SOD1*G93A mice resulted not only in a reduction of activated astrocytes and microglia in both brain stem and lumbar spinal cord but also in a rescue of neurons in the motor cortex. Moreover, behavioural tests revealed that the disease phenotype of SOD1*G93A mice is halted during treatment.Conclusion: Based on the presented results, we conclude that RD2RD2 is a potential therapeutic candidate against ALS.

Characterization of Serum Exosomes from a Transgenic Mouse Model of Alzheimer’s Disease

2019 ◽  
Vol 16 (5) ◽  
pp. 388-395 ◽  
Author(s):  
Hector Rosas-Hernandez ◽  
Elvis Cuevas ◽  
James B. Raymick ◽  
Bonnie L. Robinson ◽  
Syed F. Ali ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Amyloid Angiopathy ◽  
Western Blots ◽  
Model Of Alzheimer’S Disease ◽  
Serum Exosomes

Background: Alzheimer’s Disease (AD) is the most common type of dementia characterized by amyloid plaques containing Amyloid Beta (Aβ) peptides and neurofibrillary tangles containing tau protein. In addition to neuronal loss, Cerebral Amyloid Angiopathy (CAA) commonly occurs in AD. CAA is characterized by Aβ deposition in brain microvessels. Recent studies have suggested that exosomes (cell-derived vesicles containing a diverse cargo) may be involved in the pathogenesis of AD. Objective: Isolate and characterize brain-derived exosomes from a transgenic mouse model of AD that presents CAA. Methods: Exosomes were isolated from serum obtained from 13-month-old wild type and AD transgenic female mice using an exosome precipitation solution. Characterization of exosomal proteins was performed by western blots and dot blots. Results: Serum exosomes were increased in transgenic mice compared to wild types as determined by increased levels of the exosome markers flotillin and alix. High levels of neuronal markers were found in exosomes, without any difference any between the 2 groups. Markers for endothelial-derived exosomes were decreased in the transgenic model, while astrocytic-derived exosomes were increased. Exosome characterization showed increased levels of oligomeric Aβ and oligomeric and monomeric forms tau on the transgenic animals. Levels of amyloid precursor protein were also increased. In addition, pathological and phosphorylated forms of tau were detected, but no difference was observed between the groups. Conclusion: These data suggest that monomeric and oligomeric forms of Aβ and tau are secreted into serum via brain exosomes, most likely derived from astrocytes in the transgenic mouse model of AD with CAA. Studies on the implication of this event in the propagation of AD are underway.

scholarly journals Establishment and Characterization of a Transgenic Mouse Model for In Vivo Imaging of Bmp4 Expression in the Pancreas

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e24956 ◽  
Author(s):  
Mayu Yasunaga ◽  
Nao Oumi ◽  
Mitsuhiko Osaki ◽  
Yasuhiro Kazuki ◽  
Tomoko Nakanishi ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
In Vivo Imaging ◽  
Transgenic Mouse Model ◽  
Bmp4 Expression
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