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Search Results: 1 - 10 of 435955 matches for " Luis M. Garcia-Segura "
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Prenatal stress causes alterations in the morphology of microglia and the inflammatory response of the hippocampus of adult female mice
Yolanda Diz-Chaves, Olga Pernia, Paloma Carrero, Luis M Garcia-Segura
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-71
Abstract: Pregnant C57BL/6 mice were subjected three times/day during 45 minutes to restraint stress from gestational Day 12 to delivery. Control non-stressed pregnant mice remained undisturbed. At four months of age, non-stressed and prenatally stressed females were ovariectomized. Fifteen days after surgery, mice received an i.p. injection of vehicle or of 5?mg/kg of lipopolysaccharide (LPS). Mice were sacrificed 20 hours later by decapitation and the brains were removed. Levels of interleukin-1β (IL1β), interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), interferon γ-inducible protein 10 (IP10), and toll-like receptor 4 mRNA were assessed in the hippocampus by quantitative real-time polymerase chain reaction. Iba1 immunoreactivity was assessed by immunocytochemistry. Statistical significance was determined by one-way or two-way analysis of variance.Prenatal stress, per se, increased IL1β mRNA levels in the hippocampus, increased the total number of Iba1-immunoreactive microglial cells and increased the proportion of microglial cells with large somas and retracted cellular processes. In addition, prenatally stressed and non-stressed animals showed different responses to peripheral inflammation induced by systemic administration of LPS. LPS induced a significant increase in mRNA levels of IL-6, TNF-α and IP10 in the hippocampus of prenatally stressed mice but not of non-stressed animals. In addition, after LPS treatment, prenatally stressed animals showed a higher proportion of Iba1-immunoreactive cells in the hippocampus with morphological characteristics of activated microglia compared to non-stressed animals. In contrast, LPS induced similar increases in expression of IL1β and toll-like receptor 4 in both prenatally stressed and non-stressed animals.These findings indicate that prenatal stress induces long-lasting modifications in the inflammatory status of the hippocampus of female mice under basal conditions and alters the immune response of the hippocampus to periph
Insulin-like growth factor-I gene delivery to astrocytes reduces their inflammatory response to lipopolysaccharide
Maria J Bellini, Claudia B Here?ú, Rodolfo G Goya, Luis M Garcia-Segura
Journal of Neuroinflammation , 2011, DOI: 10.1186/1742-2094-8-21
Abstract: An adenoviral vector harboring the rat IGF-I gene and a control adenoviral vector harboring a hybrid gene encoding the herpes simplex virus type 1 thymidine kinase fused to Aequorea victoria enhanced green fluorescent protein were used in this study. Primary astrocytes from mice cerebral cortex were incubated for 24 h or 72 h with vehicle, IGF-I, the IGF-I adenoviral vector, or control vector; and exposed to bacterial lipopolysaccharide to induce an inflammatory response. IGF-I levels were measured by radioimmunoassay. Levels of interleukin 6, tumor necrosis factor-α, interleukin-1β and toll-like receptor 4 mRNA were assessed by quantitative real-time polymerase chain reaction. Levels of IGF-I receptor and IGF binding proteins 2 and 3 were assessed by western blotting. The subcellular distribution of nuclear factor κB (p65) was assessed by immunocytochemistry. Statistical significance was assessed by one way analysis of variance followed by the Bonferroni pot hoc test.IGF-I gene therapy increased IGF-I levels without affecting IGF-I receptors or IGF binding proteins. Exogenous IGF-I, and IGF-I gene therapy, decreased expression of toll-like receptor 4 and counteracted the lipopolysaccharide-induced inflammatory response of astrocytes. In addition, IGF-I gene therapy decreased lipopolysaccharide-induced translocation of nuclear factor κB (p65) to the cell nucleus.These findings demonstrate efficacy of exogenous IGF-I and of IGF-I gene therapy in reducing the inflammatory response of astrocytes. IGF-I gene therapy may represent a new approach to reduce inflammatory reactions in glial cells.As a source of growth factors and of immunologically relevant cytokines and chemokines, astrocytes play a pivotal role in the pathophysiology of neurodegenerative diseases [1-3] and in the type and extent of central nervous system immune and inflammatory responses [4]. These responses may promote tissue repair and contribute to recovery of homeostasis under acute neurodegerative con
Sex differences in the inflammatory response of primary astrocytes to lipopolysaccharide
María Santos-Galindo, Estefanía Acaz-Fonseca, María J Bellini, Luis M Garcia-Segura
Biology of Sex Differences , 2011, DOI: 10.1186/2042-6410-2-7
Abstract: Cortical astrocyte cultures were prepared from postnatal day 1 (one day after birth) male or female CD1 mice pups. In addition, cortical astrocyte cultures were also prepared from female pups that were injected at birth with 100 μg of testosterone propionate or vehicle. Cultures were treated for 5 hours with medium containing lipopolysaccharide (LPS) or with control medium. The mRNA levels of IL6, interferon-inducible protein 10 (IP10), TNFα, IL1β, Toll-like receptor 4 (TLR4), steroidogenic acute regulatory protein and translocator protein were assessed by quantitative real-time polymerase chain reaction. Statistical significance was assessed by unpaired t-test or by one-way analysis of variance followed by the Tukey post hoc test.The mRNA levels of IL6, TNFα and IL1β after LPS treatment were significantly higher in astrocytes derived from male or androgenized females compared to astrocytes derived from control or vehicle-injected females. In contrast, IP10 mRNA levels after LPS treatment were higher in astrocytes derived from control or vehicle-injected females than in those obtained from males or androgenized females. The different response of male and female astrocytes to LPS was due neither to differences in the basal expression of the inflammatory molecules nor to differences in the expression of the LPS receptor TLR4. In contrast, the different inflammatory response was associated with increased mRNA levels of translocator protein, a key steroidogenic regulator, in female astrocytes that were treated with LPS.Male and female cortical astrocytes respond differentially to an inflammatory challenge and this may be predetermined by perinatal testosterone exposure.Astrocytes, one of the glial cell types of the central nervous system (CNS), are involved in a variety of functions under physiological conditions, including the control of brain blood flow and neuronal metabolism [1,2]. In addition, astrocytes regulate extracellular potassium levels and neuronal excitabi
Neurogenin 3 Mediates Sex Chromosome Effects on the Generation of Sex Differences in Hypothalamic Neuronal Development
Maria J. Scerbo,Alejandra Freire-Regatillo,Carla D. Cisternas,Mabel Brunotto,Maria Angeles Arevalo,Luis M. Garcia-Segura,Maria J. Cambiasso
Frontiers in Cellular Neuroscience , 2014, DOI: 10.3389/fncel.2014.00188
Abstract: The organizational action of testosterone during critical periods of development is the cause of numerous sex differences in the brain. However, sex differences in neuritogenesis have been detected in primary neuronal hypothalamic cultures prepared before the peak of testosterone production by fetal testis. In the present study we assessed the hypothesis of that cell-autonomous action of sex chromosomes can differentially regulate the expression of the neuritogenic gene neurogenin 3 (Ngn3) in male and female hypothalamic neurons, generating sex differences in neuronal development. Neuronal cultures were prepared from male and female E14 mouse hypothalami, before the fetal peak of testosterone. Female neurons showed enhanced neuritogenesis and higher expression of Ngn3 than male neurons. The silencing of Ngn3 abolished sex differences in neuritogenesis, decreasing the differentiation of female neurons. The sex difference in Ngn3 expression was determined by sex chromosomes, as demonstrated using the four core genotypes mouse model, in which a spontaneous deletion of the testis-determining gene Sry from the Y chromosome was combined with the insertion of the Sry gene onto an autosome. In addition, the expression of Ngn3, which is also known to mediate the neuritogenic actions of estradiol, was increased in the cultures treated with the hormone, but only in those from male embryos. Furthermore, the hormone reversed the sex differences in neuritogenesis promoting the differentiation of male neurons. These findings indicate that Ngn3 mediates both cell-autonomous actions of sex chromosomes and hormonal effects on neuritogenesis.
Prenatal Stress Induces Long-Term Effects in Cell Turnover in the Hippocampus-Hypothalamus-Pituitary Axis in Adult Male Rats
Eva Baquedano, Cristina García-Cáceres, Yolanda Diz-Chaves, Natalia Lagunas, Isabel Calmarza-Font, I?igo Azcoitia, Luis M. Garcia-Segura, Jesús Argente, Julie A. Chowen, Laura M. Frago
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0027549
Abstract: Subchronic gestational stress leads to permanent modifications in the hippocampus-hypothalamus-pituitary-adren?alaxis of offspring probably due to the increase in circulating glucocorticoids known to affect prenatal programming. The aim of this study was to investigate whether cell turnover is affected in the hippocampus-hypothalamus-pituitary axis by subchronic prenatal stress and the intracellular mechanisms involved. Restraint stress was performed in pregnant rats during the last week of gestation (45 minutes; 3 times/day). Only male offspring were used for this study and were sacrificed at 6 months of age. In prenatally stressed adults a decrease in markers of cell death and proliferation was observed in the hippocampus, hypothalamus and pituitary. This was associated with an increase in insulin-like growth factor-I mRNA levels, phosphorylation of CREB and calpastatin levels and inhibition of calpain -2 and caspase -8 activation. Levels of the anti-apoptotic protein Bcl-2 were increased and levels of the pro-apoptotic factor p53 were reduced. In conclusion, prenatal restraint stress induces a long-term decrease in cell turnover in the hippocampus-hypothalamus-pituitary axis that might be at least partly mediated by an autocrine-paracrine IGF-I effect. These changes could condition the response of this axis to future physiological and pathophysiological situations.
Role of Neuroactive Steroids in the Peripheral Nervous System
Roberto Cosimo Melcangi,Donatella Caruso,Luis Miguel Garcia-Segura
Frontiers in Endocrinology , 2011, DOI: 10.3389/fendo.2011.00104
Abstract: Several reviews have so far pointed out on the relevant physiological and pharmacological role exerted by neuroactive steroids in the central nervous system. In the present review we summarize observations indicating that synthesis and metabolism of neuroactive steroids also occur in the peripheral nerves. Interestingly, peripheral nervous system is also a target of their action. Indeed, as here reported neuroactive steroids are physiological regulators of peripheral nerve functions and they may also represent interesting therapeutic tools for different types of peripheral neuropathy.
Estradiol Activates β-Catenin Dependent Transcription in Neurons
Olga Varea, Juan Jose Garrido, Ana Dopazo, Pablo Mendez, Luis Miguel Garcia-Segura, Francisco Wandosell
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005153
Abstract: Estradiol may fulfill a plethora of functions in neurons, in which much of its activity is associated with its capacity to directly bind and dimerize estrogen receptors. This hormone-protein complex can either bind directly to estrogen response elements (ERE's) in gene promoters, or it may act as a cofactor at non-ERE sites interacting with other DNA-binding elements such as AP-1 or c-Jun. Many of the neuroprotective effects described for estrogen have been associated with this mode of action. However, recent evidence suggests that in addition to these “genomic effects”, estrogen may also act as a more general “trophic factor” triggering cytoplasmic signals and extending the potential activity of this hormone. We demonstrated that estrogen receptor alpha associates with β-catenin and glycogen synthase kinase 3 in the brain and in neurons, which has since been confirmed by others. Here, we show that the action of estradiol activates β-catenin transcription in neuroblastoma cells and in primary cortical neurons. This activation is time and concentration-dependent, and it may be abolished by the estrogen receptor antagonist ICI 182780. The transcriptional activation of β-catenin is dependent on lymphoid enhancer binding factor-1 (LEF-1) and a truncated-mutant of LEF-1 almost completely blocks estradiol TCF-mediated transcription. Transcription of a TCF-reporter in a transgenic mouse model is enhanced by estradiol in a similar fashion to that produced by Wnt3a. In addition, activation of a luciferase reporter driven by the engrailed promoter with three LEF-1 repeats was mediated by estradiol. We established a cell line that constitutively expresses a dominant-negative LEF-1 and it was used in a gene expression microarray analysis. In this way, genes that respond to estradiol or Wnt3a, sensitive to LEF-1, could be identified and validated. Together, these data demonstrate the existence of a new signaling pathway controlled by estradiol in neurons. This pathway shares some elements of the insulin-like growth factor-1/Insulin and Wnt signaling pathways, however, our data strongly suggest that it is different from that of both these ligands. These findings may reveal a set of new physiological roles for estrogens, at least in the Central Nervous System (CNS).
Estradiol Meets Notch Signaling in Developing Neurons
María Angeles Arevalo,I?igo Azcoitia,Luis Miguel Garcia-Segura
Frontiers in Endocrinology , 2011, DOI: 10.3389/fendo.2011.00021
Abstract: The transmembrane receptor Notch, a master developmental regulator, controls gliogenesis, neurogenesis, and neurite development in the nervous system. Estradiol, acting as a hormonal signal or as a neurosteroid, also regulates these developmental processes. Here we review recent evidence indicating that estradiol and Notch signaling interact in developing hippocampal neurons by a mechanism involving the putative membrane receptor G protein-coupled receptor 30. This interaction is relevant for the control of neuronal differentiation, since the downregulation of Notch signaling by estradiol results in the upregulation of neurogenin 3, which in turn promotes dendritogenesis.
Photodissociation in proto-planetary nebulae. Hydrodynamical simulations and solutions for low-velocity multi-lobes
Guillermo Garcia-Segura
Physics , 2010, DOI: 10.1051/0004-6361/201015585
Abstract: We explore the effects of photodissociation at the stages of post-asymptotic giant branch stars to find a mechanism able to produce multi-polar shapes. We perform two-dimensional gasdynamical simulations to model the effects of photodissociation in proto-planetary nebulae. We find that post-asymptotic giant branch stars with 7,000 K or hotter are able to photodissociate a large amount of the circumstellar gas. We compute several solutions for nebulae with low-velocity multi-lobes. We find that the early expansion of a dissociation front is crucial to understand the number of lobes in proto-planetary nebulae. A dynamical instability appears when cooling is included in the swept-up molecular shell. This instability is similar to the one found in photoionization fronts, and it is associated with the thin-shell Vishniac instability. The dissociation front exacerbates the growth of the thin-shell instability, creating a fast fragmentation in shells expanding into media with power-law density distributions such as r^-2.
A wind-shell interaction model for multipolar planetary nebulae
W. Steffen,N. Koning,A. Esquivel,G. Garcia-Segura,Ma. T. Garcia-Diaz,J. A. Lopez,M. Magnor
Physics , 2013, DOI: 10.1093/mnras/stt1583
Abstract: We explore the formation of multipolar structures in planetary and pre-planetary nebulae from the interaction of a fast post-AGB wind with a highly inhomogeneous and filamentary shell structure assumed to form during the final phase of the high density wind. The simulations were performed with a new hydrodynamics code integrated in the interactive framework of the astrophysical modeling package SHAPE. In contrast to conventional astrophysical hydrodynamics software, the new code does not require any programming intervention by the user for setting up or controlling the code. Visualization and analysis of the simulation data has been done in SHAPE without external software. The key conclusion from the simulations is that secondary lobes in planetary nebulae, such as Hubble 5 and K3-17, can be formed through the interaction of a fast low-density wind with a complex high density environment, such as a filamentary circumstellar shell. The more complicated alternative explanation of intermittent collimated outflows that change direction, in many cases may therefore not be necessary. We consider that the wind-shell interaction scenario is more likely since the bow-shock shape expected from a strongly cooling bow-shock from jets is different from that of the observed bubbles. Furthermore, the timescales of the wind-wind interaction suggest that the progenitor star was rather massive.
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