scholarly journals Distinct Microglial Responses in Two Transgenic Murine Models of TAU Pathology

2018 ◽  
Vol 12 ◽  
Author(s):  
Carmen Romero-Molina ◽  
Victoria Navarro ◽  
Raquel Sanchez-Varo ◽  
Sebastian Jimenez ◽  
Juan J. Fernandez-Valenzuela ◽  
...  
Keyword(s):  
Murine Models ◽  
Tau Pathology ◽  
Transgenic Murine Models

scholarly journals Remodeling Alzheimer-amyloidosis models by seeding

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Brittany S. Ulm ◽  
David R. Borchelt ◽  
Brenda D. Moore
Keyword(s):  
Amyloid Precursor Protein ◽  
Neurodegenerative Diseases ◽  
Amyloid Beta ◽  
Precursor Protein ◽  
Time Interval ◽  
Murine Models ◽  
Brain Pathology ◽  
Amyloid Deposits ◽  
Transgenic Murine Models ◽  
Mutant Genes

AbstractAlzheimer’s disease (AD) is among the most prevalent neurodegenerative diseases, with brain pathology defined by extracellular amyloid beta deposits and intracellular tau aggregates. To aid in research efforts to improve understanding of this disease, transgenic murine models have been developed that replicate aspects of AD pathology. Familial AD is associated with mutations in the amyloid precursor protein and in the presenilins (associated with amyloidosis); transgenic amyloid models feature one or more of these mutant genes. Recent advances in seeding methods provide a means to alter the morphology of resultant amyloid deposits and the age that pathology develops. In this review, we discuss the variety of factors that influence the seeding of amyloid beta pathology, including the source of seed, the time interval after seeding, the nature of the transgenic host, and the preparation of the seeding inoculum.

Abstract 655: Determination of the pro-oncogenic role of PIM1/PIM2 kinases in male reproductive system pre-neoplastic lesions by using conditional transgenic murine models

2016 ◽  
Author(s):  
Antonio Lucena-Cacace ◽  
Manuel P Jiménez-García ◽  
Irene Ferrer ◽  
Blanca Felipe Abrio ◽  
Eva M Verdugo-Sivianes ◽  
...  
Keyword(s):  
Reproductive System ◽  
Male Reproductive System ◽  
Murine Models ◽  
Neoplastic Lesions ◽  
Transgenic Murine Models

scholarly journals Metabolic Convergence on Lipogenesis in RAS, BCR-ABL, and MYC-driven Lymphoid Malignancies

2020 ◽  
Author(s):  
Daniel Liefwalker ◽  
Meital Ryan ◽  
Ian Lai ◽  
Adriane Mosley ◽  
Gabrielle Dewson ◽  
...  
Keyword(s):  
Cell Lines ◽  
Human Subjects ◽  
Trial Registration ◽  
Metabolic Profiles ◽  
Murine Models ◽  
Clinical Interventions ◽  
Lymphoid Malignancies ◽  
Transgenic Murine Models

Abstract Background Metabolic re-programming is a central feature in many cancer subtypes and a hallmark of cancer. Many therapeutic strategies attempt to exploit this feature, although often having unintended side effects on normal metabolic programs and limited efficacy due to integrative nature of metabolic substrate sourcing. Although the initiating oncogenic lesion may vary, in lymphoid malignancies tumor cells often share similar environments and potentially similar metabolic profiles. Methods We searched publicly available data sets for common metabolic convergence in lymphoma and leukemia. Using in vitro cell lines derived in from conditional MYC, RAS, and BCR-ABL transgenic murine models we examine metabolic profiles of lipogenesis. We then utilize preclinical murine models and transgenic primary model of T-ALL to determine the effect of lipogenesis blockade across BCR-ABL, RAS, and c-MYC-driven lymphoid malignancies. Statistical significance was calculated using unpaired T tests and one-way ANOVA. Results We find that de novo lipid biogenesis is a shared feature of several lymphoma subtypes. Using cell lines derived in from conditional MYC, RAS, and BCR-ABL transgenic murine models we demonstrate shared responses to inhibition of lipogenesis by the acetyl-coA carboxylase inhibitor 5-(Tetradecloxy)-2-furic Acid (TOFA). We identify specific cell death responses to TOFA in vitro and in vivo and demonstrate delayed engraftment and progression in vivo in transplanted lymphoma cell lines. We also observed delayed progression of T-ALL in a primary transgenic mouse model upon TOFA administration. In a panel of human cell lines, we demonstrate sensitivity to TOFA treatment as a feature of MYC high expressing lymphoma cell lines. Conclusions These studies indicate that inhibition of lipogenesis may be a common survival strategy for many lymphomas and that high MYC expression is predictive of sensitivity to blockade of fatty acid synthesis. Trial Registration This study does not include any clinical interventions on human subjectsTrial RegistrationThis study does not include any clinical interventions on human subjects

Determination of the proto-oncogenic role of PIM1/PIM2 kinases in male reproductive system pre-neoplastic lesions by using conditional transgenic murine models

2016 ◽  
Vol 61 ◽  
pp. S34
Author(s):  
M.P. Jiménez-García ◽  
M.J. Robles-Frias ◽  
B. Felipe-Abrio ◽  
A. Lucena-Cacace ◽  
D. Otero-Albiol ◽  
...  
Keyword(s):  
Reproductive System ◽  
Male Reproductive System ◽  
Murine Models ◽  
Neoplastic Lesions ◽  
Transgenic Murine Models

scholarly journals Congenital Hypopituitarism: Various Genes, Various Phenotypes

2019 ◽  
Vol 51 (02) ◽  
pp. 81-90 ◽  
Author(s):  
Maria Xatzipsalti ◽  
Antonis Voutetakis ◽  
Lela Stamoyannou ◽  
George Chrousos ◽  
Christina Kanaka-Gantenbein
Keyword(s):  
Transcription Factors ◽  
Gene Mutations ◽  
Pituitary Hormones ◽  
Genetic Mutations ◽  
Murine Models ◽  
Spontaneous Mutations ◽  
Complex Disorders ◽  
Complex Process ◽  
Transgenic Murine Models ◽  
Congenital Hypopituitarism

AbstractThe ontogenesis and development of the pituitary gland is a highly complex process that depends on a cascade of transcription factors and signaling molecules. Spontaneous mutations and transgenic murine models have demonstrated a role for many of these factors, including HESX1, PROP1, PIT1, LHX3, LHX4, SOX2, SOX3, OTX2, PAX6, FGFR1, SHH, GLI2, and FGF8 in the etiology of congenital hypopituitarism. Genetic mutations in any of these factors can lead to congenital hypopituitarism, which is characterized by the deficiency in one or more pituitary hormones. The phenotype can be highly variable, consisting of isolated hypopituitarism or more complex disorders. The same phenotype can be attributed to different gene mutations; while a given gene mutation can induce different phenotypes. This review highlights the genetic variations that lead to congenital hypopituitarism and their associated defects. The overall incidence of mutations in known transcription factors in patients with hypopituitarism is low; therefore many gene mutations or even gene- epigenetic interactions have to be unraveled in the future to explain the vast majority of still unclear cases of congenital hypopituitarism.

scholarly journals A novel approach to evaluate the immunogenicity of viral antigens of clinical importance in HLA transgenic murine models

2008 ◽  
Vol 120 (1-2) ◽  
pp. 108-116 ◽  
Author(s):  
A KRISHNAN ◽  
Z WANG ◽  
T SRIVASTAVA ◽  
R RAWAL ◽  
P MANCHANDA ◽  
...  
Keyword(s):  
Clinical Importance ◽  
Murine Models ◽  
Viral Antigens ◽  
Novel Approach ◽  
Transgenic Murine Models

scholarly journals Review: Neuropathology and behavioural features of transgenic murine models of Alzheimer's disease

2017 ◽  
Vol 43 (7) ◽  
pp. 553-570 ◽  
Author(s):  
K. E. Ameen-Ali ◽  
S. B. Wharton ◽  
J. E. Simpson ◽  
P. R. Heath ◽  
P. Sharp ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Murine Models ◽  
Transgenic Murine Models

scholarly journals Esophageal functional impairments in experimental eosinophilic esophagitis

2012 ◽  
Vol 302 (11) ◽  
pp. G1347-G1355 ◽  
Author(s):  
Parm Mavi ◽  
Priya Rajavelu ◽  
Madhavi Rayapudi ◽  
Richard J. Paul ◽  
Anil Mishra
Keyword(s):  
Eosinophilic Esophagitis ◽  
Esophageal Stricture ◽  
Isometric Force ◽  
Inflammatory Cells ◽  
Esophageal Disease ◽  
Murine Models ◽  
Functional Impairments ◽  
Esophageal Dysmotility ◽  
Eosinophilic Disorders ◽  
Transgenic Murine Models

Eosinophilic esophagitis (EoE) is an emerging chronic esophageal disease. Despite the increasing diagnosis of EoE globally, the causes of EoE and other esophageal eosinophilic disorders are not clearly understood. EoE pathology includes accumulation of inflammatory cells (e.g., eosinophils, mast cells), characteristic endoscopic features (e.g., furrows, the formation of fine concentric mucosal rings, exudates), and functional impairments (e.g., esophageal stricture, dysmotility). We hypothesized that the esophageal structural pathology and functional impairments of EoE develop as a consequence of the effector functions of the accumulated inflammatory cells. We analyzed eosinophils (anti-major basic protein immunostaining), esophageal stricture (X-ray barium swallowing), and esophageal motility (isometric force) in two established transgenic murine models of EoE (CD2-IL-5 and rtTA-CC10-IL-13) and a novel eosinophil-deficient model (ΔdblGATA/CD2-IL-5). Herein, we show the following: 1) CD2-IL-5 and doxycycline (DOX)-induced rtTA-CC10-IL-13 mice have chronic eosinophilic and mast cell esophageal inflammation; 2) eosinophilic esophageal inflammation promotes esophageal stricture in both transgenic murine models; 3) the eosinophil-deficient ΔdblGATA/CD-2-IL-5 mice were protected from the induction of stricture, whereas the eosinophil-competent CD2-IL-5 mice develop esophageal stricture; 4) esophageal stricture is not reversible in DOX-induced rtTA-CC10-IL-13 mice (8 wk DOX followed by 8 wk no-DOX); and 5) IL-5 transgene-induced (CD2-IL-5) EoE evidences esophageal dysmotility (relaxation and contraction) that is independent of the eosinophilic esophageal inflammation: CD2-IL-5 and ΔdblGATA/CD2-IL-5 mice have comparable esophageal dysmotility. Collectively, our present study directly implicates chronic eosinophilic inflammation in the development of the esophageal structural impairments of experimental EoE.

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