Mouse Model of In Situ Thromboembolic Stroke and Reperfusion

Author(s):  
Orset Cyrille ◽  
Le Béhot Audrey ◽  
Bonnet Anne-Laure ◽  
Maysami Samaneh ◽  
Vivien Denis
Stroke ◽  
2011 ◽  
Vol 42 (1) ◽  
pp. 196-203 ◽  
Author(s):  
Isaac García-Yébenes ◽  
Mónica Sobrado ◽  
Juan G. Zarruk ◽  
Mar Castellanos ◽  
Natalia Pérez de la Ossa ◽  
...  

Stroke ◽  
2007 ◽  
Vol 38 (10) ◽  
pp. 2771-2778 ◽  
Author(s):  
Cyrille Orset ◽  
Richard Macrez ◽  
Alan R. Young ◽  
Didier Panthou ◽  
Eduardo Angles-Cano ◽  
...  

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii233-ii233
Author(s):  
April Bell ◽  
Lijie Zhai ◽  
Erik Ladomersky ◽  
Kristen Lauing ◽  
Lakshmi Bollu ◽  
...  

Abstract Glioblastoma (GBM) is the most common and aggressive primary central nervous system tumor in adults with a median survival of 14.6 months. GBM is a potently immunosuppressive cancer due in-part to the prolific expression of immunosuppressive indoleamine 2,3 dioxygenase 1 (IDO). Tumor cell IDO facilitates the intratumoral accumulation of regulatory T cells (Tregs; CD4+CD25+FoxP3+). Although immunosuppressive IDO activity is canonically characterized by the conversion of tryptophan into kynurenine, we have utilized transgenic and syngeneic mouse models and mutant glioma lines to demonstrate that tumor cell IDO increases Treg accumulation independent of tryptophan metabolism. Here, we address the gap in our understanding of IDO signaling activity in vivo. Subcutaneously-engrafted human GBM expressing human IDO-GFP cDNA was isolated from immunodeficient humanized NSG-SGM3 mice. The tumor was immunoprecipitated for the GFP tag using GFP-TRAP followed by mass spectrometry which revealed a novel methylation site on a lysine residue at amino acid 373 in the IDO C-terminus region. Western blot analysis of IDO protein also revealed the presence of tyrosine phosphorylation. Additionally, we recently created a new transgenic IDO reporter mouse model whereby endogenous IDO is fused to GFP via a T2A linker (IDO→GFP). This model allows for the isolation of IDO+ cells in real-time and without causing cell death, thereby creating the opportunity for downstream molecular analysis of in situ-isolated GFP+ cells. Collectively, our work suggests that IDO non-enzyme activity may involve the post-translational modifications we recently identified. As IDO activity may differ between in vitro and in vivo modeling systems, we will use the new IDO→GFP reporter mouse model for an improved mechanistic understanding of how immunosuppressive IDO facilitates Treg accumulation in vivo.


Author(s):  
Rebecca C. Lobo ◽  
Neil E. Hubbard ◽  
Patrizia Damonte ◽  
Hidetoshi Mori ◽  
Zsófia Pénzváltó ◽  
...  

PLoS ONE ◽  
2015 ◽  
Vol 10 (9) ◽  
pp. e0139089 ◽  
Author(s):  
Zhen Yang ◽  
Yunlong Zan ◽  
Xiujuan Zheng ◽  
Wangxi Hai ◽  
Kewei Chen ◽  
...  

2011 ◽  
Vol 34 (4) ◽  
pp. 935-940 ◽  
Author(s):  
Patrick M. Heiler ◽  
Friederike L. Langhauser ◽  
Friedrich Wetterling ◽  
Saema Ansar ◽  
Saskia Grudzenski ◽  
...  

2015 ◽  
Vol 256 ◽  
pp. 203-211 ◽  
Author(s):  
Yingxin Chen ◽  
Wenbin Zhu ◽  
Wenri Zhang ◽  
Nicole Libal ◽  
Stephanie J. Murphy ◽  
...  

2008 ◽  
Vol 26 (15_suppl) ◽  
pp. 17006-17006
Author(s):  
R. A. Madero-Visbal ◽  
I. C. Hernandez ◽  
J. N. Myers ◽  
C. H. Baker ◽  
T. D. Shellenberger

PLoS ONE ◽  
2015 ◽  
Vol 10 (9) ◽  
pp. e0138184 ◽  
Author(s):  
Mong-Jen Chen ◽  
Yuanqing Lu ◽  
Nicholas E. Simpson ◽  
Mark J. Beveridge ◽  
Ahmed S. Elshikha ◽  
...  

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