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Neuron and mTOR

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https://www.readbyqxmd.com/read/29453976/cell-type-specific-expression-of-constitutively-active-rheb-promotes-regeneration-of-bulbospinal-respiratory-axons-following-cervical-sci
#1
Mark W Urban, Biswarup Ghosh, Laura R Strojny, Cole G Block, Sara M Blazejewski, Megan C Wright, George M Smith, Angelo C Lepore
Damage to respiratory neural circuitry and consequent loss of diaphragm function is a major cause of morbidity and mortality in individuals suffering from traumatic cervical spinal cord injury (SCI). Repair of CNS axons after SCI remains a therapeutic challenge, despite current efforts. SCI disrupts inspiratory signals originating in the rostral ventral respiratory group (rVRG) of the medulla from their phrenic motor neuron (PhMN) targets, resulting in loss of diaphragm function. Using a rat model of cervical hemisection SCI, we aimed to restore rVRG-PhMN-diaphragm circuitry by stimulating regeneration of injured rVRG axons via targeted induction of Rheb (ras homolog enriched in brain), a signaling molecule that regulates neuronal-intrinsic axon growth potential...
February 14, 2018: Experimental Neurology
https://www.readbyqxmd.com/read/29451335/mesenchymal-stem-cells-protect-against-hypoxia-ischemia-brain-damage-by-enhancing-autophagy-through-bdnf-mtor-signaling-pathway
#2
Zhen Zheng, Li Zhang, Yi Qu, Guoguang Xiao, Shiping Li, Shan Bao, Richard Lu, Dezhi Mu
Hypoxic-ischemic encephalopathy (HIE) is a serious disease for neonates. However, present therapeutic strategies are not effective enough for treating HIE. Previous study showed that mesenchymal stem cells (MSCs) can exert neuroprotective effects for brain damage, but its mechanism remains elusive. Using in-vitro co-culture of rat cortical primary neurons and MSCs in HI conditions, we demonstrated that MSCs help increase BDNF and autophagy markers (LC3II and Beclin1) in the cultures and decrease cells death (LDH levels)...
February 16, 2018: Stem Cells
https://www.readbyqxmd.com/read/29451218/pten-knockdown-with-the-y444f-mutant-aav2-vector-promotes-axonal-regeneration-in-the-adult-optic-nerve
#3
Zheng-Ru Huang, Hai-Ying Chen, Zi-Zhong Hu, Ping Xie, Qing-Huai Liu
The lack of axonal regeneration is the major cause of vision loss after optic nerve injury in adult mammals. Activating the PI3K/AKT/mTOR signaling pathway has been shown to enhance the intrinsic growth capacity of neurons and to facilitate axonal regeneration in the central nervous system after injury. The deletion of the mTOR negative regulator phosphatase and tensin homolog (PTEN) enhances regeneration of adult corticospinal neurons and ganglion cells. In the present study, we used a tyrosine-mutated (Y444F) AAV2 vector to efficiently express a short hairpin RNA (shRNA) for silencing PTEN expression in retinal ganglion cells...
January 2018: Neural Regeneration Research
https://www.readbyqxmd.com/read/29451215/effect-of-moxibustion-on-mtor-mediated-autophagy-in-rotenone-induced-parkinson-s-disease-model-rats
#4
Shu-Ju Wang, Qi Wang, Jun Ma, Pei-Hao Yu, Zhong-Ming Wang, Bin Wang
Defects in autophagy-mediated clearance of α-synuclein may be one of the key factors leading to progressive loss of dopaminergic neurons in the substantia nigra. Moxibustion therapy for Parkinson's disease has been shown to have a positive effect, but the underlying mechanism remains unknown. Based on this, we explored whether moxibustion could protect dopaminergic neurons by promoting autophagy mediated by mammalian target of rapamycin (mTOR), with subsequent elimination of α-syn. A Parkinson's disease model was induced in rats by subcutaneous injection of rotenone at the back of their necks, and they received moxibustion at Zusanli (ST36), Guanyuan (CV4) and Fengfu (GV16), for 10 minutes at every point, once per day, for 14 consecutive days...
January 2018: Neural Regeneration Research
https://www.readbyqxmd.com/read/29449635/purkinje-cells-derived-from-tsc-patients-display-hypoexcitability-and-synaptic-deficits-associated-with-reduced-fmrp-levels-and-reversed-by-rapamycin
#5
Maria Sundberg, Ivan Tochitsky, David E Buchholz, Kellen Winden, Ville Kujala, Kush Kapur, Deniz Cataltepe, Daria Turner, Min-Joon Han, Clifford J Woolf, Mary E Hatten, Mustafa Sahin
Accumulating evidence suggests that cerebellar dysfunction early in life is associated with autism spectrum disorder (ASD), but the molecular mechanisms underlying the cerebellar deficits at the cellular level are unclear. Tuberous sclerosis complex (TSC) is a neurocutaneous disorder that often presents with ASD. Here, we developed a cerebellar Purkinje cell (PC) model of TSC with patient-derived human induced pluripotent stem cells (hiPSCs) to characterize the molecular mechanisms underlying cerebellar abnormalities in ASD and TSC...
February 15, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29447953/dendrite-growth-and-the-effect-of-ectopic-rheb-expression-on-cortical-neurons
#6
Aidan M Sokolov, Caitlin M Seluzicki, Mary C Morton, David M Feliciano
Ras homology enriched in brain (Rheb) is a GTPase that activates the protein kinase mammalian Target of Rapamycin (mTOR). Rheb mutations cause intellectual delay and megalencephaly. mTOR hyperactivation causes a constellation of neurodevelopmental disorders called "mTOR-opathies" that are frequently accompanied by hyperexcitable cortical malformations. Cortical malformations within the anterior cingulate cortex (ACC) and somatosensory cortex (SSC) frequently colocalize with hyperexcitability. Although Rheb and mTOR are implicated in the formation of cortical lesions, seizure activity, and defects in neuronal migration, the contribution of Rheb to changes in neuron size and dendrite morphology is not well established...
February 12, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29427776/beta-estradiol-and-norepinephrine-treatment-of-differentiated-sh-sy5y-cells-enhances-tau-phosphorylation-at-ser396-and-ser262-via-ampk-but-not-mtor-signaling-pathway
#7
Shohreh Majd, Zohreh Majd, Simon Koblar, John Power
Hyperphosphorylation of tau is one of the main hallmarks for Alzheimer's disease (AD) and many other tauopathies. Norepinephrine (NE), a stress-related hormone 17-β-estradiol (E2) and thought to influence tau phosphorylation (p-tau) and AD pathology. The controversy around the impact of NE and E2 requires further clarification. Moreover, the combination effect of physiological and psychological stress and estrogen alteration during menopause, which affect p-tau, has not been addressed. Exposure to E2 is believed to reduce NE release, however, the link between these two hormones and AD at cellular level was also remained unknown...
February 7, 2018: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/29421605/impaired-insulin-signaling-and-spatial-learning-in-middle-aged-rats-the-role-of-ptp1b
#8
Gabriel Keine Kuga, Vitor Rosetto Muñoz, Rafael Calais Gaspar, Susana Castelo Branco Ramos Nakandakari, Adelino Sanchez Ramos da Silva, José Diego Botezelli, José Alexandre Curiacos de Almeida Leme, Ricardo José Gomes, Leandro Pereira de Moura, Dennys Esper Cintra, Eduardo Rochete Ropelle, José Rodrigo Pauli
The insulin and Brain-Derived Neurotrophic Factor (BDNF) signaling in the hippocampus promotes synaptic plasticity and memory formation. On the other hand, aging is related to the cognitive decline and is the main risk factor for Alzheimer's Disease (AD). The Protein-Tyrosine Phosphatase 1B (PTP1B) is related to several deleterious processes in neurons and emerges as a promising target for new therapies. In this context, our study aims to investigate the age-related changes in PTP1B content, insulin signaling, β-amyloid content, and Tau phosphorylation in the hippocampus of middle-aged rats...
February 5, 2018: Experimental Gerontology
https://www.readbyqxmd.com/read/29421576/mir-93-5p-targeting-pten-regulates-the-nmda-induced-autophagy-of-retinal-ganglion-cells-via-akt-mtor-pathway-in-glaucoma
#9
Rui Li, Yiping Jin, Qian Li, Xinghuai Sun, Haohao Zhu, Hongping Cui
BACKGROUND: Glaucoma is hallmarked with the death of retinal neurons in the ganglion cell layer, which results in irreversible vision loss. The abnormal levels of miRNA have been associated with glaucoma. Our study purposed to explore the underlying molecule mechanism of miR-93-5p in NMDA-induced glaucoma. METHODS: The Sprague-Dawley (SD) rats were used for the establishment of glaucoma model with the injection of NMDA. Vision behavior test were performed on the glaucoma rats...
February 5, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29416710/developmental-and-light-regulation-of-tumor-suppressor-protein-pp2a-in-the-retina
#10
Ammaji Rajala, Yuhong Wang, Steven F Abcouwer, Thomas W Gardner, Raju V S Rajala
Protein phosphatases are a group of universal enzymes that are responsible for the dephosphorylation of various proteins and enzymes in cells. Cellular signal transduction events are largely governed by the phosphorylation of key proteins. The length of cellular response depends on the activation of protein phosphatase that dephosphorylates the phosphate groups to halt a biological response, and fine-tune the defined cellular outcome. Dysregulation of these phosphatase(s) results in various disease phenotypes...
January 5, 2018: Oncotarget
https://www.readbyqxmd.com/read/29416039/bfgf-plays-a-neuroprotective-role-by-suppressing-excessive-autophagy-and-apoptosis-after-transient-global-cerebral-ischemia-in-rats
#11
Dawei Sun, Wenying Wang, Xintao Wang, Yan Wang, Xiaotao Xu, Feng Ping, Yu Du, Wei Jiang, Derong Cui
Transient global cerebral ischemia (tGCI) is a cerebrovascular disorder that can cause apoptotic neuronal damage and functional deficits. Basic fibroblast growth factor (bFGF) was reported to be highly expressed in the central nervous system (CNS) and to exert neuroprotective effects against different CNS diseases. However, the effects of bFGF on tGCI have not been studied intensively. This study was conducted to investigate the effect of bFGF and its underlying mechanism in an animal model of tGCI. After intracerebroventricular (i...
February 7, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29416016/pharmacological-activation-of-autophagy-favors-the-clearing-of-intracellular-aggregates-of-misfolded-prion-protein-peptide-to-prevent-neuronal-death
#12
Stefano Thellung, Beatrice Scoti, Alessandro Corsaro, Valentina Villa, Mario Nizzari, Maria Cristina Gagliani, Carola Porcile, Claudio Russo, Aldo Pagano, Carlo Tacchetti, Katia Cortese, Tullio Florio
According to the "gain-of-toxicity mechanism", neuronal loss during cerebral proteinopathies is caused by accumulation of aggregation-prone conformers of misfolded cellular proteins, although it is still debated which aggregation state actually corresponds to the neurotoxic entity. Autophagy, originally described as a variant of programmed cell death, is now emerging as a crucial mechanism for cell survival in response to a variety of cell stressors, including nutrient deprivation, damage of cytoplasmic organelles, or accumulation of misfolded proteins...
February 7, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29410282/osmotic-stress-induced-toxicity-exacerbates-parkinson-s-associated-effects-via-dysregulation-of-autophagy-in-transgenic-c-elegans-model
#13
Pooja Jadiya, Snober S Mir, Aamir Nazir
The accumulation of aggregate-prone proteins is a major representative of many neurological disorders, including Parkinson's disease (PD) wherein the cellular clearance mechanisms, such as the ubiquitin-proteasome and autophagy pathways are impaired. PD, known to be associated with multiple genetic and environmental factors, is characterized by the aggregation of α-synuclein protein and loss of dopaminergic neurons in midbrain. This disease is also associated with other cardiovascular ailments. Herein, we report our findings from studies on the effect of hyper and hypo-osmotic induced toxicity representing hyper and hypotensive condition as an extrinsic epigenetic factor towards modulation of Parkinsonism, using a genetic model Caenorhabditis elegans (C...
February 2, 2018: Cellular Signalling
https://www.readbyqxmd.com/read/29385149/erythropoietin-attenuates-motor-neuron-programmed-cell-death-in-a-burn-animal-model
#14
Sheng-Hua Wu, I-Cheng Lu, Su-Shin Lee, Aij-Lie Kwan, Chee-Yin Chai, Shu-Hung Huang
Burn-induced neuromuscular dysfunction may contribute to long-term morbidity; therefore, it is imperative to develop novel treatments. The present study investigated whether erythropoietin (EPO) administration attenuates burn-induced motor neuron apoptosis and neuroinflammatory response. To validate our hypothesis, a third-degree hind paw burn rat model was developed by bringing the paw into contact with a metal surface at 75°C for 10 s. A total of 24 male Sprague-Dawley rats were randomly assigned to four groups: Group A, sham-control; Group B, burn-induced; Group C, burn + single EPO dose (5000 IU/kg i...
2018: PloS One
https://www.readbyqxmd.com/read/29378827/cilia-length-and-intraflagellar-transport-regulation-by-kinases-pkg-1-and-gck-2-in-c-elegans-sensory-neurons
#15
Muniesh Muthaiyan Shanmugam, Prerana Bhan, Hsin-Yi Huang, Jung Hsieh, Tzu-En Hua, Gong-Her Wu, Helly Punjabi, Víctor Daniel Lee Aplícano, Chih-Wei Chen, Oliver Ingvar Wagner
To understand how ciliopathies such as polycystic kidney disease or Bardet-Biedl syndrome develop, we need to understand the basic molecular mechanisms underlying cilia development. Cilia growth depends on a functional intraflagellar transport (IFT) machinery, and we hypothesized that various kinases and phosphatases might be involved in this regulatory process. A candidate screen revealed two kinases PKG-1 (a cGMP-dependent protein kinase) and GCK-2 (a MAP4K3 kinase involved in mTOR signaling) significantly affecting dye filling, chemotaxis, cilia morphology, and IFT component distribution...
January 29, 2018: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/29369005/remote-ischemic-postconditioning-protects-the-brain-from-focal-ischemia-reperfusion-injury-by-inhibiting-autophagy-through-the-mtor-p70s6k-pathway
#16
Guo-Zhong Chen, Xiao-Yun Shan, Xu-Sheng Li, Hong-Miao Tao
OBJECTIVE: Remote ischemic postconditioning (RIPostC) has been recognized as an applicable strategy for protecting against cerebral ischemia/reperfusion (I/R) injury. This study was performed to examine the effect of RIPostC on cerebral I/R and to explore its underlying mechanism. METHODS: Healthy male SD rats (N = 36) were assigned randomly into 3 groups of 12 each: sham group, I/R model group and RIPostC group. Animal models were performed by filament insertion for 2 h with middle cerebral artery occlusion(MCAO) followed by 24 h of reperfusion...
January 25, 2018: Neurological Research
https://www.readbyqxmd.com/read/29361552/the-golgi-ribbon-in-mammalian-cells-negatively-regulates-autophagy-by-modulating-mtor-activity
#17
Prajakta Gosavi, Fiona J Houghton, Paul J McMillan, Eric Hanssen, Paul A Gleeson
In vertebrates, individual Golgi stacks are joined into a compact ribbon structure, however, the relevance of a ribbon structure has been elusive. Here we exploit the finding that the membrane tether of the trans-Golgi network, GCC88, regulates the balance between Golgi mini-stacks and the Golgi ribbon. Loss of Golgi ribbons in stable cells overexpressing GCC88 resulted in compromised mechanistic target of rapamycin (mTOR) signaling and a dramatic increase in LC3-II-positive autophagosomes, whereas RNAi depletion of GCC88 restored a Golgi ribbon and reduced autophagy...
December 28, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/29360689/resveratrol-protects-early-brain-injury-after-subarachnoid-hemorrhage-by-activating-autophagy-and-inhibiting-apoptosis-mediated-by-the-akt-mtor-pathway
#18
Dan Guo, Jiangtao Xie, Junjie Zhao, Tingqin Huang, Xiaoye Guo, Jinning Song
Early brain injury (EBI) plays a key role in determining the prognosis of patients suffering from subarachnoid hemorrhage (SAH). Resveratrol, a natural polyphenol, serves a neuroprotection function on EBI after SAH. However, the potential mechanism of resveratrol on EBI remains to be elucidated. Akt, also known as protein kinase B, and mammalian target of rapamycin (mTOR), the downstream protein of Akt, play key roles in cell survival and apoptosis, cell cycle regulation, and cellular protein homeostasis. In the present study, we examined the effect of resveratrol on EBI and their potential relationship with the Akt/mTOR pathway, autophagy, and apoptosis...
January 22, 2018: Neuroreport
https://www.readbyqxmd.com/read/29358088/isogenic-fus-egfp-ipsc-reporter-lines-enable-quantification-of-fus-stress-granule-pathology-that-is-rescued-by-drugs-inducing-autophagy
#19
Lara Marrone, Ina Poser, Ian Casci, Julia Japtok, Peter Reinhardt, Antje Janosch, Cordula Andree, Hyun O Lee, Claudia Moebius, Ellen Koerner, Lydia Reinhardt, Maria Elena Cicardi, Karl Hackmann, Barbara Klink, Angelo Poletti, Simon Alberti, Marc Bickle, Andreas Hermann, Udai Pandey, Anthony A Hyman, Jared L Sterneckert
Perturbations in stress granule (SG) dynamics may be at the core of amyotrophic lateral sclerosis (ALS). Since SGs are membraneless compartments, modeling their dynamics in human motor neurons has been challenging, thus hindering the identification of effective therapeutics. Here, we report the generation of isogenic induced pluripotent stem cells carrying wild-type and P525L FUS-eGFP. We demonstrate that FUS-eGFP is recruited into SGs and that P525L profoundly alters their dynamics. With a screening campaign, we demonstrate that PI3K/AKT/mTOR pathway inhibition increases autophagy and ameliorates SG phenotypes linked to P525L FUS by reducing FUS-eGFP recruitment into SGs...
January 17, 2018: Stem Cell Reports
https://www.readbyqxmd.com/read/29351171/spinal-pkc-erk-signal-pathway-mediates-hyperalgesia-priming
#20
Wei-Hsin Chen, Ya-Ting Chang, Yong-Cyuan Chen, Sin-Jhong Cheng, Chien-Chang Chen
Chronic pain can be initiated by one or more acute stimulations to sensitize neurons into the primed state. In the primed state, the basal nociceptive thresholds of the animal are normal, but in response to another hyperalgesic stimulus, the animal develops enhanced and prolonged hyperalgesia. The exact mechanism of how primed state is formed is not completely understood. Here we showed that spinal PKC/ERK signal pathway is required for neuronal plasticity change, hyperalgesic priming formation and the development of chronic hyperalgesia using acid-induced muscle pain (AIMP) model in mice...
January 18, 2018: Pain
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