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https://www.readbyqxmd.com/read/28647594/chronic-mild-stress-impairs-latent-inhibition-and-induces-region-specific-neural-activation-in-chl1-deficient-mice-a-mouse-model-of-schizophrenia
#1
Mona Buhusi, Daniel Obray, Bret Guercio, Mitchell J Bartlett, Catalin V Buhusi
Schizophrenia is a neurodevelopmental disorder characterized by abnormal processing of information and attentional deficits. Schizophrenia has a high genetic component but is precipitated by environmental factors, as proposed by the 'two-hit' theory of schizophrenia. Here we compared latent inhibition as a measure of learning and attention, in CHL1-deficient mice, an animal model of schizophrenia, and their wild-type littermates, under no-stress and chronic mild stress conditions. All unstressed mice as well as the stressed wild-type mice showed latent inhibition...
June 21, 2017: Behavioural Brain Research
https://www.readbyqxmd.com/read/28647027/targeting-of-stem-cell-niches-using-unconventional-genetic-tools
#2
Vasily V Shinin, Andrey A Panteleyev
Maintenance of hair follicle (HF) stem cell quiescence and self-renewal are key functions of a specific cellular niche represented by the HF bulge and adjacent cell populations. The unique context of this niche is crucial for normal HF functioning, but mechanisms implicated in its maintenance are still not quite clear. The Letter to the Editor by Sada et al. introduces a novel Slc1a3-CreER genetic mouse model which, in contrast to previously reported marking tools, selectively and highly efficiently demarcates the telogen bulge inner layer, one of the critical structural components of the bulge stem cell niche...
July 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/28646094/immune-mediated-effects-targeting-hepatitis-c-virus-in-a-syngeneic-replicon-cell-transplantation-mouse-model
#3
Sepideh Levander, Fredrik Holmström, Lars Frelin, Gustaf Ahlén, Daniel Rupp, Gang Long, Ralf Bartenschlager, Matti Sällberg
OBJECTIVE: HCV is characterised by its ability to establish chronic infection in hepatocytes and to replicate in the presence of an inflammation. We mimicked this situation in vivo in immune-competent mice by syngeneic transplantation of HCV replicon-containing mouse hepatoma cells. DESIGN: A total of 5 million H-2(b) positive Hep56.1D cells, carrying a subgenomic genotype (gt) 2a replicon (HCV replicon cells) or stably expressing comparable levels of the HCV NS3/4A protease/helicase complex (NS3/4A hepatoma cells), were injected subcutaneously into syngeneic H-2(b)-restricted mice...
June 23, 2017: Gut
https://www.readbyqxmd.com/read/28646025/remodeling-of-repolarization-and-arrhythmia-susceptibility-in-a-myosin-binding-protein-c-knockout-mouse-model
#4
Amir Toib, Chen Zhang, Giulia Borghetti, Xiaoxiao Zhang, Markus Wallner, Yijun Yang, Constantine Troupes, Hajime Kubo, Thomas Sharp, Eric Feldsott, Remus M Berretta, Neil Zalavadia, Danielle Trappanese, Shavonn Harper, Polina Gross, Xiongwen Chen, Sadia Mohsin, Steven Houser
Hypertrophic cardiomyopathy (HCM) is one of the most common genetic cardiac diseases and amongst the leading causes of sudden cardiac death (SCD) in the young. The cellular mechanisms leading to SCD in HCM are not well known. Prolongation of the action potential duration (APD) is a common feature predisposing hypertrophied hearts to SCD. Previous studies have explored the roles of inward Na(+) and Ca(2+) in the development of HCM, but the role of repolarizing K(+) currents have not been defined. The objective of this study was to characterize the arrhythmogenic phenotype and cellular electrophysiological properties of mice with HCM, induced by Myosin Binding Protein C (MyBPC) Knockout (KO) and to test the hypothesis that remodeling of repolarizing K(+) currents cause APD prolongation in MyBPC KO myocytes...
June 23, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28646022/nf1-hematopoietic-cells-accelerate-malignant-peripheral-nerve-sheath-tumor-development-without-altering-chemotherapy-response
#5
Rebecca D Dodd, Chang-Lung Lee, Tess Overton, Wesley Huang, William C Eward, Lixia Luo, Yan Ma, Davis R Ingram, Keila E Torres, Diana M Cardona, Alexander Lazar, David G Kirsch
Haploinsufficiency in the tumor suppressor NF1 contributes to the pathobiology of type 1 neurofibromatosis, but a related role has not been established in malignant peripheral nerve sheath tumors (MPNST) where NF1 mutations also occur. Patients with NF1-associated MPNST appear to have worse outcomes than patients with sporadic MPNST, but the mechanism underlying this correlation is not understood. To define the impact of stromal genetics on the biology of this malignancy, we developed unique mouse models that reflect the genetics of patient-associated MPNST...
June 23, 2017: Cancer Research
https://www.readbyqxmd.com/read/28646017/ror%C3%AE-modulates-semaphorin-3e-transcription-and-neurovascular-interaction-in-pathological-retinal-angiogenesis
#6
Ye Sun, Chi-Hsiu Liu, Zhongxiao Wang, Steven S Meng, Samuel B Burnim, John Paul SanGiovanni, Theodore M Kamenecka, Laura A Solt, Jing Chen
Pathological proliferation of retinal blood vessels commonly causes vision impairment in proliferative retinopathies, including retinopathy of prematurity. Dysregulated crosstalk between the vasculature and retinal neurons is increasingly recognized as a major factor contributing to the pathogenesis of vascular diseases. Class 3 semaphorins (SEMA3s), a group of neuron-secreted axonal and vascular guidance factors, suppress pathological vascular growth in retinopathy. However, the upstream transcriptional regulators that mediate the function of SEMA3s in vascular growth are poorly understood...
June 23, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28645655/5-lipoxygenase-in-monocytes-emerges-as-a-therapeutic-target-for-intimal-hyperplasia-in-a-murine-wire-injured-femoral-artery
#7
Seung Eun Baek, Min A Jang, Seung Jin Lee, So Youn Park, Sun Sik Bae, Chi Dae Kim
Given the importance of leukotrienes in vascular inflammation induced by local tissue injury, this study investigated the role for 5-lipoxygenase (5-LO) in monocytes in the development of intimal hyperplasia. As a mechanistic study, the importance of monocyte 5-LO in monocyte-macrophage differentiation with subsequent infiltration in neointima was evaluated. In a mouse model of wire-injured femoral artery, intimal hyperplasia started as early as 2 wks after injury, and luminal area and blood flow were reduced due to increased neointima formation...
June 20, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28645539/gli1-labeled-adult-mesenchymal-stem-progenitor-cells-and-hedgehog-signaling-contribute-to-endochondral-heterotopic-ossification
#8
Chen Kan, Lijun Chen, Yangyang Hu, Na Ding, Yuyun Li, Tammy L McGuire, Haimei Lu, John A Kessler, Lixin Kan
Heterotopic ossification (HO), acquired or hereditary, endochondral or intramembranous, is the formation of true bone outside the normal skeleton. Since perivascular Gli1+ progenitors contribute to injury induced organ fibrosis, and CD133 is expressed by a variety of populations adult stem cells, this study utilized Cre-lox based genetic lineage tracing to test the contribution to endochondral HO of adult stem/progenitor cells that expressed either Gli1 or CD133. We found that both lineages contributed broadly to different normal tissues with distinct patterns, but that only Gli1-creERT labeled stem/progenitor cells contributed to all stages of endochondral HO in a BMP dependent, injury induced, transgenic mouse model...
June 20, 2017: Bone
https://www.readbyqxmd.com/read/28644737/circulatory-cnp-rescues-craniofacial-hypoplasia-in-achondroplasia
#9
S Yamanaka, Kazumasa Nakao, N Koyama, Y Isobe, Y Ueda, Y Kanai, E Kondo, T Fujii, M Miura, A Yasoda, Kazuwa Nakao, K Bessho
Achondroplasia is the most common genetic form of human dwarfism, characterized by midfacial hypoplasia resulting in occlusal abnormality and foramen magnum stenosis, leading to serious neurologic complications and hydrocephalus. Currently, surgery is the only way to manage jaw deformity, neurologic complications, and hydrocephalus in patients with achondroplasia. We previously showed that C-type natriuretic peptide (CNP) is a potent stimulator of endochondral bone growth of long bones and vertebrae and is also a potent stimulator in the craniofacial region, which is crucial for midfacial skeletogenesis...
June 1, 2017: Journal of Dental Research
https://www.readbyqxmd.com/read/28644379/physical-forces-may-cause-the-hoxd-gene-cluster-elongation
#10
Spyros Papageorgiou
Hox gene collinearity was discovered be Edward B. Lewis in 1978. It consists of the Hox1, Hox2, Hox3 ordering of the Hox genes in the chromosome from the telomeric to the centromeric side of the chromosome. Surprisingly, the spatial activation of the Hox genes in the ontogenetic units of the embryo follows the same ordering along the anterior-posterior embryonic axis. The chromosome microscale differs from the embryo macroscale by 3 to 4 orders of magnitude. The traditional biomolecular mechanisms are not adequate to comprise phenomena at so divergent spatial domains...
June 23, 2017: Biology
https://www.readbyqxmd.com/read/28644148/5-azacytidine-promotes-invadopodia-formation-and-tumor-metastasis-through-the-upregulation-of-pi3k-in-ovarian-cancer-cells
#11
Dan Cao, Dan Li, Yong Huang, Yu Ma, Binglan Zhang, Chengjian Zhao, Senyi Deng, Min Luo, Tao Yin, Yu-Quan Wei, Wei Wang
The high incidence of metastasis accounts for most of the lethality of ovarian cancer. Invadopodia are small, specialized types of machinery that degrade the extracellular matrix and are thus involved in the invasion and metastasis of cancer cells. The formation of invadopodia is regulated by both genetic and epigenetic factors. However, the ways by which methylation/demethylation regulates the dynamics of invadopodia in ovarian cancer are largely unknown. In this study, we found that the inhibition of methylation by 5-AZ (5-Azacytidine) increased the formation of invadopodia and enhanced degradation of the extracellular matrix in ovarian cancer cells...
June 20, 2017: Oncotarget
https://www.readbyqxmd.com/read/28643912/mouse-models-for-the-study-of-cranial-base-growth-and-anomalies
#12
REVIEW
S R Vora
The cranial base is a central and integral component of the cranioskeleton, yet little is known about its growth. Despite the dissimilarities between human and murine cranioskeletal form, mouse models are proving instrumental in studying craniofacial growth. The objectives of this review are to summarize recent findings from numerous mouse models that display growth defects in one or more cranial base synchondroses, with accompanying changes in chondrocyte cellular zones. Many of these models also display altered growth of the cranial vault and/or the facial region...
June 2017: Orthodontics & Craniofacial Research
https://www.readbyqxmd.com/read/28642245/a-reporter-mouse-model-for-in-vivo-tracing-and-in-vitro-molecular-studies-of-melanocytic-lineage-cells-and-their-diseases
#13
Melissa Crawford, Valerie Leclerc, Lina Dagnino
Alterations in melanocytic lineage cells give rise to a plethora of distinct human diseases, including neurocristopathies, cutaneous pigmentation disorders, loss of vision and hearing, as well as melanoma. Understanding the ontogeny and biology of melanocytic cells, as well as how they interact with their surrounding environment, are key steps in the development of therapies for diseases that involve this cell lineage. Efforts to culture and characterize primary melanocytes from normal or genetically engineered mouse models have at times yielded contrasting observations...
June 22, 2017: Biology Open
https://www.readbyqxmd.com/read/28642195/how-lipid-droplets-tag-along-glycerolipid-synthetic-enzymes-and-lipid-storage
#14
REVIEW
Huan Wang, Michael V Airola, Karen Reue
Triacylglycerols (TAG) serve as the predominant form of energy storage in mammalian cells, and TAG synthesis influences conditions such as obesity, fatty liver, and insulin resistance. In most tissues, the glycerol 3-phosphate pathway enzymes are responsible for TAG synthesis, and the regulation and function of these enzymes is therefore important for metabolic homeostasis. Here we review the sites and regulation of glycerol-3-phosphate acyltransferase (GPAT), acylglycerol-3-phosphate acyltransferase (AGPAT), lipin/phosphatidic acid phosphatase (PAP), and diacylglycerol acyltransferase (DGAT) enzyme action...
June 19, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28642124/identification-of-genetic-variants-associated-with-huntington-s-disease-progression-a-genome-wide-association-study
#15
Davina J Hensman Moss, Antonio F Pardiñas, Douglas Langbehn, Kitty Lo, Blair R Leavitt, Raymund Roos, Alexandra Durr, Simon Mead, Peter Holmans, Lesley Jones, Sarah J Tabrizi
BACKGROUND: Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. METHODS: We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008-11)...
June 19, 2017: Lancet Neurology
https://www.readbyqxmd.com/read/28641540/metallothionein-is-a-potential-therapeutic-strategy-for-amyotrophic-lateral-sclerosis
#16
Shin-Ichi Ono
Lou Gehrig's disease, a synonym of amyotrophic lateral sclerosis, is an adult-onset lethal neurodegenerative disorder. Irrespective of extensive efforts to elucidate the pathogenesis of the disease and searches for therapies, no favorable pharmacotherapeutic strategies have yet to be proposed. In a popular rodent model of ALS, G93A SOD1 mice, intracellular copper conditions were geared toward copper accumulation inside cells, resulting in an acceleration of oxidative stress and apoptotic process. Disruption of intracellular copper homeostasis was common to transgenic mice expressing human mutant SOD1s...
June 22, 2017: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28641308/detection-of-phosphatidylserine-positive-exosomes-for-the-diagnosis-of-early-stage-malignancies
#17
Raghava Sharma, Xianming Huang, Rolf A Brekken, Alan J Schroit
BACKGROUND: There has been increasing interest in the detection of tumour exosomes in blood for cancer diagnostics. Most studies have focussed on miRNA and protein signatures that are surrogate markers for specific tumour types. Because tumour cells and tumour-derived exosomes display phosphatidylserine (PS) in their outer membrane leaflet, we developed a highly sensitive ELISA-based system that detects picogram amounts of exosomal phospholipid in plasma as a cancer biomarker. METHODS: This report describes the development of a highly specific and sensitive ELISA for the capture of PS-expressing tumour exosomes in the blood of tumour-bearing mice...
June 22, 2017: British Journal of Cancer
https://www.readbyqxmd.com/read/28640447/role-of-serca-pump-in-muscle-thermogenesis-and-metabolism
#18
Muthu Periasamy, Santosh Kumar Maurya, Sanjaya Kumar Sahoo, Sushant Singh, Sanjaya Kumar Sahoo, Felipe C G Reis, Naresh Chandra Bal
In muscle cells, the sarcoplasmic reticulum (SR) not only acts as a Ca2+ store, but also regulates the contractile characteristics of the muscle. Ca2+ release from the SR is the primary mechanism for activating muscle contraction and reuptake of Ca2+ by the sarcoplasmic reticulum Ca2+ ATPase (SERCA) pump causes muscle relaxation. The SERCA pump isoforms are encoded by three genes, SERCA 1, 2, and 3, which are differentially expressed in muscle and determine SR Ca2+ dynamics by affecting the rate and amount of Ca2+ uptake, thereby affecting SR store and release of Ca2+ in muscle...
June 18, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28639940/genetic-specification-of-left-right-asymmetry-in-the-diaphragm-muscles-and-their-motor-innervation
#19
Camille Charoy, Sarah Dinvaut, Yohan Chaix, Laurette Morlé, Isabelle Sanyas, Muriel Bozon, Karine Kindbeiter, Bénédicte Durand, Jennifer M Skidmore, Lies De Groef, Motoaki Seki, Lieve Moons, Christiana Ruhrberg, James F Martin, Donna M Martin, Julien Falk, Valerie Castellani
The diaphragm muscle is essential for breathing in mammals. Its asymmetric elevation during contraction correlates with morphological features suggestive of inherent left-right (L/R) asymmetry. Whether this asymmetry is due to L versus R differences in the muscle or in the phrenic nerve activity is unknown. Here, we have combined the analysis of genetically modified mouse models with transcriptomic analysis to show that both the diaphragm muscle and phrenic nerves have asymmetries, which can be established independently of each other during early embryogenesis in pathway instructed by Nodal, a morphogen that also conveys asymmetry in other organs...
June 22, 2017: ELife
https://www.readbyqxmd.com/read/28639695/glycogen-synthase-kinase-3%C3%AE-ablation-limits-pancreatitis-induced-acinar-to-ductal-metaplasia
#20
Li Ding, Geou-Yarh Liou, Daniel M Schmitt, Peter Storz, Jin-San Zhang, Daniel D Billadeau
Acinar-to-ductal metaplasia (ADM) is a reversible epithelial trans-differentiation process that occurs in the pancreas in response to acute inflammation. ADM can rapidly progress toward pre-malignant pancreatic intraepithelial neoplasia (PanIN) lesions in the presence of mutant KRas and ultimately pancreatic adenocarcinoma (PDAC). In the present work we elucidate the role and related mechanism of glycogen synthase kinase-3beta (GSK-3β) in ADM development using in vitro 3D cultures and genetically engineered mouse models...
June 22, 2017: Journal of Pathology
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