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  1. Article ; Online: Method for organotypic tissue culture in the aged animal

    Jared Schommer / Matthew Schrag / Alexander Nackenoff / Gurdeep Marwarha / Othman Ghribi

    MethodsX, Vol 4, Iss C, Pp 166-

    2017  Volume 171

    Abstract: Organotypic slicing of brain tissue from young rodents has been used as a powerful model system for biomedical research [1–3]. Organotypic slicing complements cell culture and in vivo studies in multiple facets. This system can be useful for ... ...

    Abstract Organotypic slicing of brain tissue from young rodents has been used as a powerful model system for biomedical research [1–3]. Organotypic slicing complements cell culture and in vivo studies in multiple facets. This system can be useful for investigating manipulation of cellular signaling pathways without the hindrance of the blood-brain barrier while sacrificing fewer animals in the process. It also allows for preserved cellular connectivity and local intact circuitry which is a drawback of isolated cell cultures. Studies on age-related diseases have mainly used embryonic or early postnatal organotypic slice tissue. Excluding synaptic plasticity studies that are usually carried-out over a few hours and use adult mice or rats, a handful of studies performed on adult animals have had success for survival of slices [4,5]. Here we describe a method for culturing organotypic slices with high viability from hippocampus of aged mice and rabbits. • Our method permits slices from mice as old as 16 months and rabbits as old as years of age to survive ex vivo up to 8 weeks [6–9]. Such a slice system may be relevant to investigating age-related brain diseases.
    Keywords We are describing a method for organotypic tissue culture in the aged animal in this manuscript ; Science ; Q
    Language English
    Publishing date 2017-01-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article: Maternal low-protein diet decreases brain-derived neurotrophic factor expression in the brains of the neonatal rat offspring

    Marwarha, Gurdeep / Jared Schommer / Kate Claycombe-Larson / Othman Ghribi

    Journal of nutritional biochemistry. 2017 July, v. 45

    2017  

    Abstract: Prenatal exposure to a maternal low-protein (LP) diet has been known to cause cognitive impairment, learning and memory deficits. However, the underlying mechanisms have not been identified. Herein, we demonstrate that a maternal LP diet causes, in the ... ...

    Abstract Prenatal exposure to a maternal low-protein (LP) diet has been known to cause cognitive impairment, learning and memory deficits. However, the underlying mechanisms have not been identified. Herein, we demonstrate that a maternal LP diet causes, in the brains of the neonatal rat offspring, an attenuation in the basal expression of the brain-derived neurotrophic factor (BDNF), a neurotrophin indispensable for learning and memory. Female rats were fed either a 20% normal protein (NP) diet or an 8% LP 3 weeks before breeding and during the gestation period. Maternal LP diet caused a significant reduction in the Bdnf expression in the brains of the neonatal rats. We further found that the maternal LP diet reduced the activation of the cAMP/protein kinase A/cAMP response element binding protein (CREB) signaling pathway. This reduction was associated with a significant decrease in CREB binding to the Bdnf promoters. We also show that prenatal exposure to the maternal LP diet results in an inactive or repressed exon I and exon IV promoter of the Bdnf gene in the brain, as evidenced by fluxes in signatory hallmarks in the enrichment of acetylated and trimethylated histones in the nucleosomes that envelop the exon I and exon IV promoters, causing the Bdnf gene to be refractory to transactivation. Our study is the first to determine the impact of a maternal LP diet on the basal expression of BDNF in the brains of the neonatal rats exposed prenatally to an LP diet.
    Keywords binding proteins ; brain ; breeding ; cAMP-dependent protein kinase ; cyclic AMP ; exons ; females ; genes ; gestation period ; histones ; low protein diet ; maternal exposure ; memory ; memory disorders ; neonates ; nucleosomes ; progeny ; rats ; signal transduction ; transcriptional activation
    Language English
    Dates of publication 2017-07
    Size p. 54-66.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 1014929-6
    ISSN 1873-4847 ; 0955-2863
    ISSN (online) 1873-4847
    ISSN 0955-2863
    DOI 10.1016/j.jnutbio.2017.03.005
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 5044: Show issues

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  3. Article: Palmitate-induced Endoplasmic Reticulum stress and subsequent C/EBPα Homologous Protein activation attenuates leptin and Insulin-like growth factor 1 expression in the brain

    Marwarha, Gurdeep / David Collins / Jared Schommer / Kate Claycombe / Othman Ghribi

    Cellular Signaling. 2016 Nov., v. 28, no. 11

    2016  

    Abstract: The peptide hormones Insulin-like growth factor-1 (IGF1) and leptin mediate a myriad of biological effects - both in the peripheral and central nervous systems. The transcription of these two hormones is regulated by the transcription factor C/EBPα, ... ...

    Abstract The peptide hormones Insulin-like growth factor-1 (IGF1) and leptin mediate a myriad of biological effects - both in the peripheral and central nervous systems. The transcription of these two hormones is regulated by the transcription factor C/EBPα, which in turn is negatively regulated by the transcription factor C/EBP Homologous Protein (CHOP), a specific marker of endoplasmic reticulum (ER) stress. In the peripheral system, disturbances in leptin and IGF-1 levels are implicated in a variety of metabolic diseases including obesity, diabetes, atherosclerosis and cardiovascular diseases. Current research suggests a positive correlation between consumption of diets rich in saturated free fatty acids (sFFA) and metabolic diseases. Induction of ER stress and subsequent dysregulation in the expression levels of leptin and IGF-1 have been shown to mediate sFFA-induced metabolic diseases in the peripheral system. Palmitic acid (palmitate), the most commonly consumed sFFA, has been shown to be up-taken by the brain, where it may promote neurodegeneration. However, the extent to which palmitate induces ER stress in the brain and attenuates leptin and IGF1 expression has not been determined. We fed C57BL/6J mice a palmitate-enriched diet and determined effects on the expression levels of leptin and IGF1 in the hippocampus and cortex. We further determined the extent to which ER stress and subsequent CHOP activation mediate the palmitate effects on the transcription of leptin and IGF1. We demonstrate that palmitate induces ER stress and decreases leptin and IGF1 expression by inducing the expression of CHOP. The molecular chaperone 4-phenylbutyric acid (4-PBA), an inhibitor of ER stress, precludes the palmitate-evoked down-regulation of leptin and IGF1 expression. Furthermore, the activation of CHOP in response to ER stress is pivotal in the attenuation of leptin and IGF1 expression as knocking-down CHOP in mice or in SH-SY5Y and Neuro-2a (N2a) cells rescues the palmitate-induced mitigation in leptin and IGF1 expression. Our study implicates for the first time ER stress-induced CHOP activation in the brain as a mechanistic link in the palmitate-induced negative regulation of leptin and IGF1, two neurotrophic cytokines that play an indispensable role in the mammalian brain.
    Keywords cell communication ; cortex ; cytokines ; diet ; endoplasmic reticulum ; endoplasmic reticulum stress ; free fatty acids ; hippocampus ; insulin-like growth factor I ; leptin ; mice ; molecular chaperones ; neurodegenerative diseases ; palmitates ; palmitic acid ; transcription (genetics) ; transcription factors
    Language English
    Dates of publication 2016-11
    Size p. 1789-1805.
    Document type Article
    ZDB-ID 1002702-6
    ISSN 0898-6568
    ISSN 0898-6568
    DOI 10.1016/j.cellsig.2016.08.012
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2579: Show issues Location:
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  4. Article ; Online: Silencing GADD153/CHOP gene expression protects against Alzheimer's disease-like pathology induced by 27-hydroxycholesterol in rabbit hippocampus.

    Jaya R P Prasanthi / Tyler Larson / Jared Schommer / Othman Ghribi

    PLoS ONE, Vol 6, Iss 10, p e

    2011  Volume 26420

    Abstract: Endoplasmic reticulum (ER) stress is suggested to play a key role in the pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD). Sustained ER stress leads to activation of the growth arrest and leucine zipper transcription factor, ... ...

    Abstract Endoplasmic reticulum (ER) stress is suggested to play a key role in the pathogenesis of neurodegenerative diseases including Alzheimer's disease (AD). Sustained ER stress leads to activation of the growth arrest and leucine zipper transcription factor, DNA damage inducible gene 153 (gadd153; also called CHOP). Activated gadd153 can generate oxidative damage and reactive oxygen species (ROS), increase β-amyloid (Aβ) levels, disturb iron homeostasis and induce inflammation as well as cell death, which are all pathological hallmarks of AD. Epidemiological and laboratory studies suggest that cholesterol dyshomeostasis contributes to the pathogenesis of AD. We have previously shown that the cholesterol oxidized metabolite 27-hydroxycholesterol (27-OHC) triggers AD-like pathology in organotypic slices. However, the extent to which gadd153 mediates 27-OHC effects has not been determined. We silenced gadd153 gene with siRNA and determined the effects of 27-OHC on AD hallmarks in organotypic slices from adult rabbit hippocampus. siRNA to gadd153 reduced 27-OHC-induced Aβ production by mechanisms involving reduction in levels of β-amyloid precursor protein (APP) and β-secretase (BACE1), the enzyme that initiates cleavage of APP to yield Aβ peptides. Additionally, 27-OHC-induced tau phosphorylation, ROS generation, TNF-α activation, and iron and apoptosis-regulatory protein levels alteration were also markedly reduced by siRNA to gadd153. These data suggest that ER stress-mediated gadd153 activation plays a central role in the triggering of AD pathological hallmarks that result from incubation of hippocampal slices with 27-OHC. Our results add important insights into cellular mechanisms that underlie the potential contribution of cholesterol metabolism in AD pathology, and suggest that preventing gadd153 activation protects against AD related to cholesterol oxidized products.
    Keywords Medicine ; R ; Science ; Q
    Subject code 572
    Language English
    Publishing date 2011-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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