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axon transport

Yan-Rong Zheng, Xiang-Nan Zhang, Zhong Chen
Axonal mitochondrial quality is essential for neuronal health and functions. Compromised mitochondrial quality, reflected by loss of membrane potential, collapse of ATP production, abnormal morphology, burst of reactive oxygen species generation, and impaired Ca2+ buffering capacity, can alter mitochondrial transport. Mitochondrial transport in turn maintains axonal mitochondrial homeostasis in several ways. Newly generated mitochondria are anterogradely transported along with axon from soma to replenish axonal mitochondrial pool, while damaged mitochondria undergo retrograde transport for repair or degradation...
March 21, 2019: CNS Neuroscience & Therapeutics
Amy E Rumora, Giovanni LoGrasso, John M Hayes, Faye E Mendelson, Maegan A Tabbey, Julia A Haidar, Stephen I Lentz, Eva L Feldman
Neuropathy is the most common complication of prediabetes and diabetes and presents as distal-to-proximal loss of peripheral nerve function in the lower extremities. Neuropathy progression and disease severity in prediabetes and diabetes correlates with dyslipidemia in man and murine models of disease. Dyslipidemia is characterized by elevated levels of circulating saturated fatty acids (SFAs) that associate with the progression of neuropathy. Increased intake of monounsaturated fatty acid (MUFA)-rich diets confers metabolic health benefits; however, the impact of fatty acid saturation in neuropathy is unknown...
March 18, 2019: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Angela R Dixon, Eric N Horst, Jeniffer J Garcia, Patricia R Ndjouyep-Yamaga, Geeta Mehta
Burgeoning use of segregated microfluidic platforms that parse somas and neurites into discrete compartments is fueling unique examinations of neuronal structure and physiology in a manner impossible to achieve with non-compartmentalized systems. However, even though this line of axon-soma polarizing microfluidic devices stems from the same general design of a Campenot chamber set-up, slight deviations in device geometry appear to induce vastly different nutrient transport profiles that influence neuron survival and maturation...
March 15, 2019: Neuroscience Letters
David Bartolomé-Martín, Ignacio Ibáñez, Dolores Piniella, Elena Martínez-Blanco, Sara G Pelaz, Francisco Zafra
Dopamine and glutamate transporters (DAT and GLT-1, respectively) share some biophysical characteristics, as both are secondary active carriers coupled to electrochemical ion gradients. In order to identify common or specific components of their respective proteomes, we performed a proximity labelling assay (BioID) in the hippocampal cell line HT22. While most of the identified proteins were specific for each transporter (and will be analyzed elsewhere), we detected two membrane proteins in the shared interactome of GLT-1 and DAT: the transmembrane protein 263 (Tmem263) and the potassium channel protein Kv7...
March 15, 2019: Neuropharmacology
Melvin R Hayden, DeAna G Grant, Annayya R Aroor, Vincent G DeMarco
Type 2 diabetes is associated with diabetic cognopathy. Anti-hyperglycemic sodium glucose transporter 2 (SGLT2) inhibitors have shown promise in reducing cognitive impairment in mice with type 2 diabetes mellitus. We recently described marked ultrastructural (US) remodeling of the neurovascular unit (NVU) in type 2 diabetic db / db female mice. Herein, we tested whether the SGLT-2 inhibitor, empagliflozin (EMPA), protects the NVU from abnormal remodeling in cortical gray and subcortical white matter. Ten-week-old female wild-type and db / db mice were divided into lean controls (CKC, n = 3), untreated db / db (DBC, n = 3), and EMPA-treated db / db (DBE, n = 3)...
March 7, 2019: Brain Sciences
Diogo Trigo, Maria B Goncalves, Jonathan P T Corcoran
Neuronal regeneration is a highly energy-demanding process that greatly relies on axonal mitochondrial transport to meet the enhanced metabolic requirements. Mature neurons typically fail to regenerate after injury, partly because of mitochondrial motility and energy deficits in injured axons. Retinoic acid receptor (RAR)-β signaling is involved in axonal and neurite regeneration. Here we investigate the effect of RAR-β signaling on mitochondria trafficking during neurite outgrowth and find that it enhances their proliferation, speed, and movement toward the growing end of the neuron via hypoxia-inducible factor 1α signaling...
March 11, 2019: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Minjie He, Yan Lin, Yuzhen Xu
Colorectal cancer (CRC) is a highly malignant gastrointestinal tumor accompanied by poor prognosis. Long non-coding RNA (lncRNA) plays an important role in the progression and physiology of tumors as it competes with endogenous RNAs, including miRNA and mRNA. In the present study, a multi-step computational method was used to build a CRC-related functional lncRNA-mediated competitive endogenous RNA (ceRNA) network (LMCN). lncRNAs with more degrees and betweenness centrality (BC) were screened out as hub lncRNAs...
March 2019: Oncology Letters
Hamish Crerar, Emily Scott-Solomon, Chantal Bodkin-Clarke, Catia Andreassi, Maria Hazbon, Emilie Logie, Marifé Cano-Jaimez, Marco Gaspari, Rejji Kuruvilla, Antonella Riccio
Neurons are extraordinarily large and highly polarized cells that require rapid and efficient communication between cell bodies and axons over long distances. In peripheral neurons, transcripts are transported along axons to growth cones, where they are rapidly translated in response to extrinsic signals. While studying Tp53inp2, a transcript highly expressed and enriched in sympathetic neuron axons, we unexpectedly discovered that Tp53inp2 is not translated. Instead, the transcript supports axon growth in a coding-independent manner...
February 27, 2019: Neuron
Ameya Sanjay Kasture, Daniela Bartel, Thomas Steinkellner, Sonja Sucic, Thomas Hummel, Michael Freissmuth
The serotonin transporter (SERT) regulates serotonergic neurotransmission by retrieving released serotonin and replenishing vesicular stores. SERT is not only delivered to axons but it is also present on the neuronal soma and on dendrites. It has not been possible to restrict the distribution of SERT without affecting transporter function. Hence, the physiological role of somatodendritic SERT remains enigmatic. The SERT C-terminus harbors a conserved RI-motif, which recruits SEC24C, a cargo receptor in the coatomer protein-II coat...
March 6, 2019: Neuropharmacology
Fangchao Liu, Yanhua Zhang, Janelle Schafer, Guangzhao Mao, Harry G Goshgarian
CONTEXT: Following a spinal cord hemisection at the second cervical segment the ipsilateral hemidiaphragm is paralyzed due to the disruption of the rostral ventral respiratory group (rVRG) axons descending to the ipsilateral phrenic motoneurons (PN). Systemically administered theophylline activates a functionally latent crossed phrenic pathway (CPP) which decussates caudal to the hemisection and activates phrenic motoneurons ipsilateral to the hemisection. The result is return of function to the paralyzed hemidiaphragm...
March 7, 2019: Journal of Spinal Cord Medicine
Haruki Nishimura, Makoto Kawasaki, Hitoshi Suzuki, Takanori Matsuura, Yasuhito Motojima, Hideo Ohnishi, Yoshiaki Yamanaka, Mitsuhiro Yoshimura, Takashi Maruyama, Reiko Saito, Hiromichi Ueno, Satomi Sonoda, Kazuaki Nishimura, Tatsushi Onaka, Yoichi Ueta, Akinori Sakai
Despite the high incidence of neuropathic pain, its mechanism remains unclear. Oxytocin (OXT) is an established endogenous polypeptide produced in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus. OXT, which is synthesized by OXT neurons in the SON and the magnocellular part of the PVN (mPVN), is delivered into the posterior pituitary (PP), then released into the systemic blood circulation. Meanwhile, OXT-containing neurosecretory cells in the parvocellular part of the PVN (pPVN) are directly projected to the spinal cord and are associated with sensory modulation...
February 28, 2019: Neuroscience
Jui-Hu Shih, Chuang-Hsin Chiu, Kuo-Hsing Ma, Yuahn-Sieh Huang, Chyng-Yann Shiue, Ting-Yin Yeh, Li-Ting Kao, Yang-Yi Lin, I-Hsun Li
The 3,4-methylenedioxymethamphetamine (MDMA) is a popular recreational drug, which ultimately leads to serotonergic (5-HT) neurotoxicity and psychiatric disorders. Previous in vitro studies have consistently demonstrated that MDMA provokes autophagic activation, as well as damage of 5-HT axons and nerve fibers. So far, whether autophagy, a well-conserved cellular process that is critical for cell fate, also participates in MDMA-induced neurotoxicity in vivo remains elusive. Here, we first examined time-course of autophagy-related changes during repeated administration of MDMA (10 mg/kg s...
February 28, 2019: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
Ariel Ionescu, Tal Gradus, Topaz Altman, Roy Maimon, Noi Saraf Avraham, Michal Geva, Michael Hayden, Eran Perlson
Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease affecting both the upper and lower motor neurons (MNs), with no effective treatment currently available. Early pathological events in ALS include perturbations in axonal transport (AT), formation of toxic protein aggregates and Neuromuscular Junction (NMJ) disruption, which all lead to axonal degeneration and motor neuron death. Pridopidine is a small molecule that has been clinically developed for Huntington disease. Here we tested the efficacy of pridopidine for ALS using in vitro and in vivo models...
March 1, 2019: Cell Death & Disease
Göker Arpağ, Stephen R Norris, S Iman Mousavi, Virupakshi Soppina, Kristen J Verhey, William O Hancock, Erkan Tüzel
Intracellular cargo transport by kinesin family motor proteins is crucial for many cellular processes, particularly vesicle transport in axons and dendrites. In a number of cases, the transport of specific cargo is carried out by two classes of kinesins that move at different speeds and thus compete during transport. Despite advances in single-molecule characterization and modeling approaches, many questions remain regarding the effect of intermotor tension on motor attachment/reattachment rates during cooperative multimotor transport...
February 5, 2019: Biophysical Journal
Mariana Bertini Teixeira, Marcos Rodrigo Alborghetti, Jörg Kobarg
Fasciculation and elongation zeta/zygin (FEZ) proteins are a family of hub proteins and share many characteristics like high connectivity in interaction networks, they are involved in several cellular processes, evolve slowly and in general have intrinsically disordered regions. In 1985, unc-76 gene was firstly described and involved in axonal growth in C. elegans , and in 1997 Bloom and Horvitz enrolled also the human homologues genes, FEZ1 and FEZ2 , in this process. While nematodes possess one gene ( unc-76 ), mammalians have one more copy ( FEZ1 and FEZ2 )...
February 21, 2019: World Journal of Biological Chemistry
Johnathan Cooper-Knock, Tobias Moll, Tennore Ramesh, Lydia Castelli, Alexander Beer, Henry Robins, Ian Fox, Isabell Niedermoser, Philip Van Damme, Matthieu Moisse, Wim Robberecht, Orla Hardiman, Monica P Panades, Abdelilah Assialioui, Jesus S Mora, A Nazli Basak, Karen E Morrison, Christopher E Shaw, Ammar Al-Chalabi, John E Landers, Matthew Wyles, Paul R Heath, Adrian Higginbottom, Theresa Walsh, Mbombe Kazoka, Christopher J McDermott, Guillaume M Hautbergue, Janine Kirby, Pamela J Shaw
Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disorder without effective neuroprotective therapy. Known genetic variants impair pathways, including RNA processing, axonal transport, and protein homeostasis. We report ALS-causing mutations within the gene encoding the glycosyltransferase GLT8D1. Exome sequencing in an autosomal-dominant ALS pedigree identified p.R92C mutations in GLT8D1, which co-segregate with disease. Sequencing of local and international cohorts demonstrated significant ALS association in the same exon, including additional rare deleterious mutations in conserved amino acids...
February 26, 2019: Cell Reports
Marco Tulio Núñez, Cecilia Hidalgo
Iron and calcium share the common feature of being essential for normal neuronal function. Iron is required for mitochondrial function, synaptic plasticity, and the development of cognitive functions whereas cellular calcium signals mediate neurotransmitter exocytosis, axonal growth and synaptic plasticity, and control the expression of genes involved in learning and memory processes. Recent studies have revealed that cellular iron stimulates calcium signaling, leading to downstream activation of kinase cascades engaged in synaptic plasticity...
2019: Frontiers in Neuroscience
Mingjun Tang, Ziming Luo, Yihui Wu, Jing Zhuang, Kaijing Li, Dongpeng Hu, Huifeng Rong, Bikun Xian, Jian Ge
BACKGROUND: BAM15 is a novel mitochondrial protonophore uncoupler capable of protecting mammals from acute renal ischemic-reperfusion injury and cold-induced microtubule damage. The purpose of our study was to investigate the effect of BAM15 on apoptosis during 5-day transportation of human-induced pluripotent stem (hiPS)-differentiated retinal tissue. METHODS: Retinal tissues of 30 days and 60 days were transported with or without BAM15 for 5 days in the laboratory or by real express...
February 22, 2019: Stem Cell Research & Therapy
Livia Goto-Silva, Marisa P McShane, Sara Salinas, Yannis Kalaidzidis, Giampietro Schiavo, Marino Zerial
Long-distance axonal trafficking plays a critical role in neuronal function and transport defects have been linked to neurodegenerative disorders. Various lines of evidence suggest that the small GTPase Rab5 plays a role in neuronal signaling via early endosomal transport. Here, we characterized the motility of Rab5 endosomes in primary cultures of mouse hippocampal pyramidal cells by live-cell imaging and showed that they exhibit bi-directional long-range motility in axons, with a strong bias toward retrograde transport...
February 21, 2019: Scientific Reports
Rajaneesh Gupta, Pampa Saha, Tanusree Sen, Nilkantha Sen
Traumatic Brain Injury (TBI) affects more than 1.7 million Americans each year and about 30% of TBI-patients having visual impairments. The loss of retinal ganglion cells (RGC) in the retina and axonal degeneration in the optic nerve have been attributed to vision impairment following TBI; however, the molecular mechanism has not been elucidated. Here we have shown that an increase in histone di-methylation at lysine 9 residue (H3K9Me2), synthesized by the catalytic activity of a histone methyltransferase, G9a is responsible for RGC loss and axonal degeneration in the optic nerve following TBI...
February 18, 2019: Free Radical Biology & Medicine
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