Analysis of Apolipoprotein A5, C3, and Plasma Triglyceride Concentrations in 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.

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

Scientific Reports ◽

10.1038/s41598-021-94307-0 ◽

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.

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Psychiatric disorders and impairments in GABAergic neurotransmission: approaches using genetically engineered mice

Neuroscience Research ◽

10.1016/j.neures.2009.09.1514 ◽

2009 ◽

Vol 65 ◽

pp. S8

Author(s):

Yuchio Yanagawa

Keyword(s):

Psychiatric Disorders ◽

Genetically Engineered ◽

Gabaergic Neurotransmission ◽

Genetically Engineered Mice

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

Molecular Cancer Therapeutics ◽

10.1158/1535-7163.mct-10-0207 ◽

2010 ◽

Vol 9 (8) ◽

pp. 2354-2364 ◽

Cited By ~ 23

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

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

Journal of Experimental Medicine ◽

10.1084/jem.20101823 ◽

2011 ◽

Vol 208 (6) ◽

pp. 1189-1201 ◽

Cited By ~ 528

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.

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