Psychosocial stress-induced brain atrophy and its suppression via theanine intake
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PROVIDER: PRJNA493551 | ENA |
REPOSITORIES: ENA
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Project description:When mice of accelerated senescence prone 10 (SAMP10) were psychosocially stressed using male mouse’s territorial imperative, the mice exhibited higher cerebral atrophy and cognitive dysfunction than same-aged group-housing mice. The brain atrophy was examined using MRI. The volumes of various brain areas were decreased at the time of one month after confrontational housing. However, in SAMP10 mice ingesting theanine, the main amino acid in tea leaves, brain atrophy was suppressed even under confrontational housing. To investigate the function of theanine, the early response against stress was examined at the third day of confrontational housing. The level of transcription factor Npas4 that plays a role in the development of inhibitory synapses for regulating the balance between excitation and suppression was significantly increased by theanine intake. Actually, the levels of glutamate and γ-aminobutyric acid (GABA), excitatory and inhibitory neurotransmitters, were balanced in the mice ingested theanine under confrontational housing. These data suggest that theanine suppresses stress-induced damage in the brain via increased expression of Npas4 and regulation of excitement/suppression balance. In addition, SAMP10 is a useful model of stress vulnerability.
2018-09-28 | GSE120546 | GEO
Project description:Genistein is one of the flabonoids which is included in high concentration in soy and has a high estrogenic activity. Beneficial effects of estrogen or hormone replacement therapy (HRT) on muscle mass or muscle atrophy have been demonstrated. We investigated the preventive effects and underlying mechanisms of genistein intake on denervation-induced muscle atrophy. Genistein intake significantly suppressed the loss of soleus muscle weight and the denervation-induced up-regulations of FOXO1 protein. The results of a DNA microarray showed that the estrogen receptor (ER) target genes are changed by genistein intake. Genistein suppressed the soleus muscle atrophy, and it was attenuated under the ER antagonist treatment. The administration of an ERα agonist suppressed the denervation-induced muscle atrophy and up-regulation of Atrogin1 gene expression, but the ERβ agonist had no effect.
2016-01-23 | GSE77121 | GEO
Project description:In the present study, we investigated the consequences of trehalose intake on brain metabolism in mice drinking for 0, 1, and 10 days. Microarray analyses were performed to identify the molecular targets involved in the brain metabolism of trehalose intake.
2019-04-01 | GSE112976 | GEO
Project description:Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) impacts human health beyond acute infection. Myalgia and fatigue represent two of the most prevalent symptoms in post-COVID-19 syndrome. To determine the mechanisms underlying prolonged muscle symptoms, we characterized longitudinal histopathological and transcriptional changes of skeletal muscle after acute respiratory SARS-CoV-2 infection in a COVID-19 hamster model and compared them with respiratory influenza A virus (IAV) infection. Histopathological and bulk RNA sequencing analyses at 3, 30, and 60 days post infection (dpi) showed no evidence of direct viral invasion, inflammatory cell infiltration, or microthrombi in skeletal muscle, but myofiber atrophy was observed in the SARS-CoV-2 group at 60 dpi, accompanied by downregulation of myofiber genes, atrogenes, and cytoplasmic ribosomal protein genes, and upregulation of autophagy genes. There was persistent downregulation of genes involved in mitochondrial oxidative phosphorylation, fatty acid beta-oxidation, and tricarboxylic acid cycle in the SARS-CoV-2 but not the IAV group. Moreover, TNF-alpha/NF-kB and TGF-beta signaling pathways were differentially regulated in the SARS-CoV-2 group. Our findings suggest that persistent muscle symptoms after COVID-19 may be caused by muscle atrophy and energy metabolism suppression, and that the systemic inflammatory cytokine response may contribute, in part, to the skeletal muscle abnormalities.
2024-06-28 | GSE231910 | GEO
Project description:Skeletal muscle atrophy is a debilitating condition associated with weakness, fatigue, and reduced functional capacity. Nuclear factor-kappaB (NF-κB) transcription factors play a critical role in atrophy. Knockout of genes encoding p50 or the NF-κB co-transactivator, Bcl-3, abolish disuse atrophy and thus they are NF-κB factors required for disuse atrophy. We do not know however, the genes targeted by NF-κB that produce the atrophied phenotype. Here we identify the genes required to produce disuse atrophy using gene expression profiling in wild type compared to Nfkb1 (gene encodes p50) and Bcl-3 deficient mice. There were 185 and 240 genes upregulated in wild type mice due to unloading, that were not upregulated in Nfkb1-/- and Bcl-3-/- mice, respectively, and so these genes were considered direct or indirect targets of p50 and Bcl-3. All of the p50 gene targets were contained in the Bcl-3 gene target list. Most genes were involved with protein degradation, signaling, translation, transcription, and transport. To identify direct targets of p50 and Bcl-3 we performed chromatin immunoprecipitation of selected genes previously shown to have roles in atrophy. Trim63 (MuRF1), Fbxo32 (MAFbx), Ubc, Ctsl, Runx1, Tnfrsf12a (Tweak receptor), and Cxcl10 (IP-10) showed increased Bcl-3 binding to κB sites in unloaded muscle and thus were direct targets of Bcl-3. p50 binding to the same sites on these genes either did not change or increased, supporting the idea of p50:Bcl-3 binding complexes. p65 binding to κB sites showed decreased or no binding to these genes with unloading. Fbxo9, Psma6, Psmc4, Psmg4, Foxo3, Ankrd1 (CARP), and Eif4ebp1 did not show changes in p65, p50, or Bcl-3 binding to κB sites, and so were considered indirect targets of p50 and Bcl-3. This work represents the first study to use a global approach to identify genes required to produce the atrophied phenotype with disuse. 24 mice were used based on 4 mice per group, 3 mouse genotypes (wild type, Nfkb1-/-, Bcl3-/-) and 2 conditions (weight-bearing and unloaded).
2011-01-10 | E-GEOD-23497 | biostudies-arrayexpress
Project description:We here longitudinally investigated how spinal muscular atrophy (SMA) and nusinersen shaped local immune responses in the cerebrospinal fluid (CSF).
2024-04-20 | PXD051600 | Pride
Project description:To elaborate the process of denervated muscular atrophy, and provide scientific basis for the prevention and treatment of denervated muscular atrophy. we performed a time course transcriptomic analysis of denervated muscular atrophy
2019-06-16 | E-MTAB-8009 | biostudies-arrayexpress
Project description:The TGFβ cytokine family member, GDF15, reduces food intake and body weight and represents a potential treatment for obesity. Because the brain stem-restricted expression pattern of its receptor, GDNF Family Receptor α–like (GFRAL), presents an exciting opportunity to understand mechanisms of action for area postrema neurons in food intake, we generated GfralCre and conditional GfralCreERT mice to visualize and manipulate GFRAL neurons. We found infection or pathophysiologic states (rather than meal ingestion) stimulate GFRAL neurons. TRAP-Seq analysis of GFRAL neurons revealed their expression of a wide range of neurotransmitters and neuropeptides. Artificially activating GfralCre-expressing neurons inhibited feeding, decreased gastric emptying, and promoted a conditioned taste aversion (CTA). GFRAL neurons most strongly innervate the parabrachial nucleus (PBN), where they target CGRP-expressing (CGRPPBN) neurons. Silencing CGRPPBN neurons abrogated the aversive and anorexic effects of GDF-15. These findings suggest that GFRAL neurons link non-meal-associated, pathophysiologic signals to suppress nutrient uptake and absorption.
2021-01-01 | GSE160257 | GEO
Project description:Belt electrode-skeletal muscle electrical stimulation (B-SES) involves the use of belt-shaped electrodes to simultaneously contract multiple muscle groups. Twitch contractions have been demonstrated to protect against denervation-induced muscle atrophy in rats, possibly via mitochondrial biosynthesis. In this study, we examined whether inducing tetanus contractions with B-SES suppresses muscle atrophy and identified the underlying molecular mechanisms. We evaluated the effects of acute (60 Hz, 5 min) and chronic (60 Hz, 5 min, every alternate day for 1 week) B-SES on the tibialis anterior (TA) and gastrocnemius (GAS) muscles in Sprague Dawley rats using belt electrodes attached to both ankle joints. In acute stimulation, a significant decrease in glycogen content in the left and right TA and GAS was observed, suggesting that B-SES causes simultaneous contractions in multiple muscle groups. B-SES also enhanced p70S6K phosphorylation, an indicator of the mechanistic target of rapamycin complex 1 activity. During chronic stimulations, rats were divided into control (CONT), denervation-induced atrophy (DEN), and DEN+electrically stimulated with B-SES (DEN＋ES) groups. After 7 days of treatment, muscle wet weight (n = 8-11 for each group) and muscle fiber cross-sectional area (CSA, n = 6 for each group) of the TA and GAS muscles were reduced in the DEN and DEN+ES groups compared to those in the CON group. The DEN+ES group showed significantly higher muscle weight and CSA than the DEN group. Although RNA-seq and pathway analysis suggested that mitochondrial and ribosome biogenesis are key events in this phenomenon, mitochondrial content showed no difference. In contrast, ribosomal RNA 28S and 45S (n = 6) levels in the DEN+ES group were higher than those in the DEN group. The mRNA levels of the muscle proteolytic molecules Atrogin-1 and MuRF1 were significantly higher in DEN than in CONT but were suppressed in DEN+ES. In conclusion, tetanic electrical stimulation of both ankles using belt electrodes was effective in preventing denervation-induced atrophy in multiple muscle groups. Unlike twitch contractions, ribosomal biosynthesis plays a key role in tetanic contractions to prevent muscle atrophy.
2024-01-06 | E-MTAB-13286 | biostudies-arrayexpress
Project description:Spinal muscular atrophy (SMA) is a common genetic motor neuron (MN) disease caused by low levels of the ubiquitously expressed housekeeping survival motor neuron (SMN) protein, whereas concomitant overexpression of plastin 3 (PLS3) protects from SMA. Here we identify neurocalcin delta (NCALD), a neuronal calcium sensor, as a second fully protective SMA modifier, which counteracts SMA pathology when downregulated. We show reduced Ca2+ influx and impaired endocytosis in SMA, which are crucial processes in synaptic vesicle recycling and neurotransmission. Remarkably, both reduced NCALD or increased PLS3 restore endocytosis in cell culture and MN function across species in zebrafish, worm and mouse SMA models, whereas Ca2+ influx remains disturbed. Furthermore, NCALD physically binds clathrin in a Ca2+-dependent manner. We propose that NCALD acts as a Ca2+-regulated inhibitor of endocytosis, and that endocytosis is critically affected in SMA. This finding opens new therapeutic avenues for SMA. Multifactorial design comparing affected patients and unaffected disease carriers against severly affected control group to identify disease modifying transcripts
2015-01-01 | E-GEOD-58316 | biostudies-arrayexpress