Murine models of inflammation: role of CD23

Allergy ◽  
2000 ◽  
Vol 55 (suppl 61) ◽  
pp. 21-26 ◽  
Author(s):  
Y. Riffo-Vasquez ◽  
S. Pitchford ◽  
D. Spina
Keyword(s):  
Murine Models

scholarly journals Targeting HSPA1A in ARID2-deficient lung adenocarcinoma

2021 ◽  
Author(s):  
Xue Wang ◽  
Yuetong Wang ◽  
Zhaoyuan Fang ◽  
Hua Wang ◽  
Jian Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Genetically Engineered ◽  
Malignant Progression ◽  
Murine Models ◽  
Rna Seq ◽  
Potential Therapeutic Target ◽  
Lung Cancers ◽  
Integrative Analyses

Abstract Somatic mutations of the chromatin remodeling gene ARID2 are observed in about 7% of human lung adenocarcinoma (LUAD). However, the role of ARID2 in the pathogenesis of LUAD remains largely unknown. Here we find that ARID2 expression is decreased during the malignant progression of both human and mice LUAD. Using two KrasG12D-based genetically engineered murine models (GEMM), we demonstrate that ARID2 knockout significantly promotes lung cancer malignant progression and shortens the overall survival. Consistently, ARID2 knockdown significantly promotes cell proliferation in human and mice lung cancer cells. Through integrative analyses of Chip-Seq and RNA-Seq data, we find that Hspa1a is up-regulated by Arid2 loss. Knockdown of Hspa1a specifically inhibits malignant progression of Arid2-deficient but not Arid2-wt lung cancers in both cell lines as well as animal models. Treatment with Hspa1a inhibitor could significantly inhibit the malignant progression of lung cancer with Arid2 deficiency. Together, our findings establish ARID2 as an important tumor suppressor in LUAD with novel mechanistic insights, and further identify HSPA1A as a potential therapeutic target in ARID2-deficient LUAD.

A Role of Plasminogen in Atherosclerosis and Restenosis Models in Mice

1999 ◽  
Vol 82 (S 01) ◽  
pp. 4-7 ◽  
Author(s):  
Victoria A. Ploplis ◽  
Steven Busuttil ◽  
Peter Carmeliet ◽  
Desire Collen ◽  
Edward F. Plow
Keyword(s):  
Vessel Wall ◽  
Inflammatory Responses ◽  
Leukocyte Migration ◽  
Early Event ◽  
Macrophage Migration ◽  
Murine Models ◽  
Response Models ◽  
Deficient Mice

SummaryIn addition to its preeminent role in fibrinolysis, the plasminogen system is believed to play a key role in mediating cell migration. Leukocyte migration into the vessel wall is a key and early event in the development of the lesions of atherosclerosis and restenosis, pathologies which may be viewed as specific examples of vascular inflammatory responses. The development of mice in which the plasminogen gene has been inactivated affords an opportunity to test the contribution of plasminogen in leukocyte migration during in vivo. This article summarizes recent studies conducted in murine models of the inflammatory repsonse, restenosis and atherosclerosis in which leukocyte migration, and in particular monocyte/macrophage migration, has been evaluated in plasminogen-deficient mice. Recruitment of these cells through the vessel wall in inflammatory response models and into the vessel wall in restenosis and transplant atherosclerosis models is substantially blunted. These data implicate plasminogen in the migration of leukocytes in these murine models. With the numerous correlations between components and/or activation of the plasminogen system in restenosis and atherosclerosis, these results also support a role of plasminogen in the corresponding human pathologies.

scholarly journals The in vivo ISGylome links ISG15 to metabolic pathways and autophagy upon Listeria monocytogenes infection

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Yifeng Zhang ◽  
Fabien Thery ◽  
Nicholas C. Wu ◽  
Emma K. Luhmann ◽  
Olivier Dussurget ◽  
...  
Keyword(s):  
Listeria Monocytogenes ◽  
Metabolic Pathways ◽  
Quantitative Proteomics ◽  
Computational Analysis ◽  
Murine Models ◽  
Direct Modification ◽  
Catalytic Sites ◽  
Listeria Monocytogenes Infection

AbstractISG15 is an interferon-stimulated, ubiquitin-like protein, with anti-viral and anti-bacterial activity. Here, we map the endogenous in vivo ISGylome in the liver following Listeria monocytogenes infection by combining murine models of reduced or enhanced ISGylation with quantitative proteomics. Our method identifies 930 ISG15 sites in 434 proteins and also detects changes in the host ubiquitylome. The ISGylated targets are enriched in proteins which alter cellular metabolic processes, including upstream modulators of the catabolic and antibacterial pathway of autophagy. Computational analysis of substrate structures reveals that a number of ISG15 modifications occur at catalytic sites or dimerization interfaces of enzymes. Finally, we demonstrate that animals and cells with enhanced ISGylation have increased basal and infection-induced autophagy through the modification of mTOR, WIPI2, AMBRA1, and RAB7. Taken together, these findings ascribe a role of ISGylation to temporally reprogram organismal metabolism following infection through direct modification of a subset of enzymes in the liver.

scholarly journals The Representative Porcine Model for Human Cardiovascular Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Yoriyasu Suzuki ◽  
Alan C. Yeung ◽  
Fumiaki Ikeno
Keyword(s):  
Animal Models ◽  
Porcine Model ◽  
Small Animal ◽  
Large Animal ◽  
Murine Models ◽  
Practical Applications ◽  
Large Animal Models ◽  
Small Animal Models ◽  
Insight Into

To improve human health, scientific discoveries must be translated into practical applications. Inherent in the development of these technologies is the role of preclinical testing using animal models. Although significant insight into the molecular and cellular basis has come from small animal models, significant differences exist with regard to cardiovascular characteristics between these models and humans. Therefore, large animal models are essential to develop the discoveries from murine models into clinical therapies and interventions. This paper will provide an overview of the more frequently used large animal models, especially porcine models for preclinical studies.

Role of interleukin-18 in experimental infections with Streptococcus pneumoniae

2005 ◽  
Vol 54 (4) ◽  
pp. 323-326 ◽  
Author(s):  
G K Paterson ◽  
C E Blue ◽  
T J Mitchell
Keyword(s):  
Streptococcus Pneumoniae ◽  
Pneumococcal Pneumonia ◽  
Infection Type ◽  
Bacterial Species ◽  
Murine Models ◽  
Positive Bacterium ◽  
Nasopharyngeal Colonization ◽  
Complex Influence ◽  
Multifunctional Cytokine

IL-18, a multifunctional cytokine, has been shown to be involved in the immune response to numerous pathogens including several bacterial species. To study its role in infection by the Gram-positive bacterium Streptococcus pneumoniae, wild-type and IL-18 knockout BALB/c mice were compared in murine models of pneumococcal pneumonia, bacteraemia and nasopharyngeal colonization. The influence of IL-18 varied with the infection type, whereby it contributed to increased bacterial loads in pneumonia, reduced levels of colonization and had no effect on levels of bacteraemia following intravenous challenge. Likewise, the influence of IL-18 on pneumonia varied between two infecting pneumococcal strains. Comparison of these results with previous data also suggested that the influence of IL-18 in pneumococcal pneumonia differs with the mouse strain genetic background. Overall, these results demonstrate the complex influence of IL-18 in the response to the pneumococcus.

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