scholarly journals Development of a transplantable glioma tumour model from genetically engineered mice: MRI/MRS/MRSI characterisation

2016 ◽  
Vol 129 (1) ◽  
pp. 67-76 ◽  
Author(s):  
Magdalena Ciezka ◽  
Milena Acosta ◽  
Cristina Herranz ◽  
Josep M. Canals ◽  
Martí Pumarola ◽  
...  
Keyword(s):  
Genetically Engineered ◽  
Tumour Model ◽  
Genetically Engineered Mice

scholarly journals Toxicity modelling of Plk1-targeted therapies in genetically engineered mice and cultured primary mammalian cells

2011 ◽  
Vol 2 (1) ◽  
Author(s):  
Monika Raab ◽  
Sven Kappel ◽  
Andrea Krämer ◽  
Mourad Sanhaji ◽  
Yves Matthess ◽  
...  
Keyword(s):  
Targeted Therapies ◽  
Mammalian Cells ◽  
Genetically Engineered ◽  
Genetically Engineered Mice

scholarly journals Tenascin-C in Heart Diseases—The Role of Inflammation

2021 ◽  
Vol 22 (11) ◽  
pp. 5828
Author(s):  
Kyoko Imanaka-Yoshida
Keyword(s):  
Ventricular Remodeling ◽  
Heart Diseases ◽  
Genetically Engineered ◽  
Matricellular Protein ◽  
Myocardial Repair ◽  
Inflammatory Reactions ◽  
Tenascin C ◽  
Genetically Engineered Mice

Tenascin-C (TNC) is a large extracellular matrix (ECM) glycoprotein and an original member of the matricellular protein family. TNC is transiently expressed in the heart during embryonic development, but is rarely detected in normal adults; however, its expression is strongly up-regulated with inflammation. Although neither TNC-knockout nor -overexpressing mice show a distinct phenotype, disease models using genetically engineered mice combined with in vitro experiments have revealed multiple significant roles for TNC in responses to injury and myocardial repair, particularly in the regulation of inflammation. In most cases, TNC appears to deteriorate adverse ventricular remodeling by aggravating inflammation/fibrosis. Furthermore, accumulating clinical evidence has shown that high TNC levels predict adverse ventricular remodeling and a poor prognosis in patients with various heart diseases. Since the importance of inflammation has attracted attention in the pathophysiology of heart diseases, this review will focus on the roles of TNC in various types of inflammatory reactions, such as myocardial infarction, hypertensive fibrosis, myocarditis caused by viral infection or autoimmunity, and dilated cardiomyopathy. The utility of TNC as a biomarker for the stratification of myocardial disease conditions and the selection of appropriate therapies will also be discussed from a clinical viewpoint.

scholarly journals Characterization and visualization of murine coagulation factor VIII-producing cells in vivo

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Morisada Hayakawa ◽  
Asuka Sakata ◽  
Hiroko Hayakawa ◽  
Hikari Matsumoto ◽  
Takafumi Hiramoto ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Factor Viii ◽  
Fluorescent Protein ◽  
Coagulation Factor ◽  
Coagulation Factors ◽  
Genetically Engineered ◽  
Coagulation Factor Viii ◽  
Liver Sinusoidal Endothelial Cells ◽  
Genetically Engineered Mice

AbstractCoagulation factors are produced from hepatocytes, whereas production of coagulation factor VIII (FVIII) from primary tissues and cell species is still controversial. Here, we tried to characterize primary FVIII-producing organ and cell species using genetically engineered mice, in which enhanced green fluorescent protein (EGFP) was expressed instead of the F8 gene. EGFP-positive FVIII-producing cells existed only in thin sinusoidal layer of the liver and characterized as CD31high, CD146high, and lymphatic vascular endothelial hyaluronan receptor 1 (Lyve1)+. EGFP-positive cells can be clearly distinguished from lymphatic endothelial cells in the expression profile of the podoplanin− and C-type lectin-like receptor-2 (CLEC-2)+. In embryogenesis, EGFP-positive cells began to emerge at E14.5 and subsequently increased according to liver maturation. Furthermore, plasma FVIII could be abolished by crossing F8 conditional deficient mice with Lyve1-Cre mice. In conclusion, in mice, FVIII is only produced from endothelial cells exhibiting CD31high, CD146high, Lyve1+, CLEC-2+, and podoplanin− in liver sinusoidal endothelial cells.

scholarly journals Immune Competency of a Hairless Mouse Strain for Improved Preclinical Studies in Genetically Engineered Mice

2010 ◽  
Vol 9 (8) ◽  
pp. 2354-2364 ◽  
Author(s):  
Beverly S. Schaffer ◽  
Marcia H. Grayson ◽  
Joy M. Wortham ◽  
Courtney B. Kubicek ◽  
Amanda T. McCleish ◽  
...  
Keyword(s):  
Mouse Strain ◽  
Hairless Mouse ◽  
Genetically Engineered ◽  
Preclinical Studies ◽  
Genetically Engineered Mice ◽  
Immune Competency

scholarly journals miR-146a is a significant brake on autoimmunity, myeloproliferation, and cancer in mice

2011 ◽  
Vol 208 (6) ◽  
pp. 1189-1201 ◽  
Author(s):  
Mark P. Boldin ◽  
Konstantin D. Taganov ◽  
Dinesh S. Rao ◽  
Lili Yang ◽  
Jimmy L. Zhao ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Immune Cell ◽  
Myeloid Cell ◽  
Genetically Engineered ◽  
Biological Processes ◽  
Targeted Deletion ◽  
Genetically Engineered Mice ◽  
Immune Defects ◽  
Molecular Brake

Excessive or inappropriate activation of the immune system can be deleterious to the organism, warranting multiple molecular mechanisms to control and properly terminate immune responses. MicroRNAs (miRNAs), ∼22-nt-long noncoding RNAs, have recently emerged as key posttranscriptional regulators, controlling diverse biological processes, including responses to non-self. In this study, we examine the biological role of miR-146a using genetically engineered mice and show that targeted deletion of this gene, whose expression is strongly up-regulated after immune cell maturation and/or activation, results in several immune defects. Collectively, our findings suggest that miR-146a plays a key role as a molecular brake on inflammation, myeloid cell proliferation, and oncogenic transformation.

scholarly journals Elucidating the role of Agl in bladder carcinogenesis by generation and characterization of genetically engineered mice

2018 ◽  
Vol 40 (1) ◽  
pp. 194-201
Author(s):  
Joseph L Sottnik ◽  
Vandana Mallaredy ◽  
Ana Chauca-Diaz ◽  
Carolyn Ritterson Lew ◽  
Charles Owens ◽  
...  
Keyword(s):  
Glycogen Storage Disease Type ◽  
Gene Signature ◽  
Glycogen Storage ◽  
Genetically Engineered ◽  
Normal Bladder ◽  
Populations At Risk ◽  
Genetically Engineered Mice ◽  
Patient Prognosis ◽  
The Impact

AbstractAmylo-α-1,6-glucosidase,4-α-glucanotransferase (AGL) is an enzyme primarily responsible for glycogen debranching. Germline mutations lead to glycogen storage disease type III (GSDIII). We recently found AGL to be a tumor suppressor in xenograft models of human bladder cancer (BC) and low levels of AGL expression in BC are associated with poor patient prognosis. However, the impact of low AGL expression on the susceptibility of normal bladder to carcinogenesis is unknown. We address this gap by developing a germline Agl knockout (Agl−/−) mouse that recapitulates biochemical and histological features of GSDIII. Agl−/− mice exposed to N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) had a higher BC incidence compared with wild-type mice (Agl+/+). To determine if the increased BC incidence observed was due to decreased Agl expression in the urothelium specifically, we developed a urothelium-specific conditional Agl knockout (Aglcko) mouse using a Uroplakin II-Cre allele. BBN-induced carcinogenesis experiments repeated in Aglcko mice revealed that Aglcko mice had a higher BC incidence than control (Aglfl/fl) mice. RNA sequencing revealed that tumors from Agl−/− mice had 19 differentially expressed genes compared with control mice. An ‘Agl Loss’ gene signature was developed and found to successfully stratify normal and tumor samples in two BC patient datasets. These results support the role of AGL loss in promoting carcinogenesis and provide a rationale for evaluating Agl expression levels, or Agl Loss gene signature scores, in normal urothelium of populations at risk of BC development such as older male smokers.

scholarly journals Development of Genetically Engineered Mice Lacking All Three Nitric Oxide Synthases

2006 ◽  
Vol 102 (2) ◽  
pp. 147-154 ◽  
Author(s):  
Masato Tsutsui ◽  
Hiroaki Shimokawa ◽  
Tsuyoshi Morishita ◽  
Yasuhide Nakashima ◽  
Nobuyuki Yanagihara
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthases ◽  
Genetically Engineered ◽  
Genetically Engineered Mice
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