scholarly journals Vesicular Transport of Encapsulated microRNA between Glial and Neuronal Cells

2020 ◽  
Vol 21 (14) ◽  
pp. 5078 ◽  
Author(s):  
Walter J. Lukiw ◽  
Aileen I. Pogue
Keyword(s):  
Information Transfer ◽  
Biological Information ◽  
Messenger Rnas ◽  
Innate Immune Signaling ◽  
Cells Of Origin ◽  
Metabolic Products ◽  
Inflammatory Phenotype ◽  
The Central Nervous System ◽  
Neuro Inflammation ◽  
End Stage

Exosomes (EXs) and extracellular microvesicles (EMVs) represent a diverse assortment of plasma membrane-derived nanovesicles, 30–1000 nm in diameter, released by all cell lineages of the central nervous system (CNS). They are examples of a very active and dynamic form of extracellular communication and the conveyance of biological information transfer essential to maintain homeostatic neurological functions and contain complex molecular cargoes representative of the cytoplasm of their cells of origin. These molecular cargoes include various mixtures of proteins, lipids, proteolipids, cytokines, chemokines, carbohydrates, microRNAs (miRNA) and messenger RNAs (mRNA) and other components, including end-stage neurotoxic and pathogenic metabolic products, such as amyloid beta (Aβ) peptides. Brain microglia, for example, respond to both acute CNS injuries and degenerative diseases with complex reactions via the induction of a pro-inflammatory phenotype, and secrete EXs and EMVs enriched in selective pathogenic microRNAs (miRNAs) such as miRNA-34a, miRNA-125b, miRNA-146a, miRNA-155, and others that are known to promote neuro-inflammation, induce complement activation, disrupt innate–immune signaling and deregulate the expression of neuron-specific phosphoproteins involved in neurotropism and synaptic signaling. This communication will review our current understanding of the trafficking of miRNA-containing EXs and EMVs from astrocytes and “activated pro-inflammatory” microglia to target neurons in neurodegenerative diseases with an emphasis on Alzheimer’s disease wherever possible.

scholarly journals Biodiversity of CS–proteoglycan sulphation motifs: chemical messenger recognition modules with roles in information transfer, control of cellular behaviour and tissue morphogenesis

2018 ◽  
Vol 475 (3) ◽  
pp. 587-620 ◽  
Author(s):  
Anthony Hayes ◽  
Kazuyuki Sugahara ◽  
Brooke Farrugia ◽  
John M. Whitelock ◽  
Bruce Caterson ◽  
...  
Keyword(s):  
Information Transfer ◽  
Enzyme Inhibitors ◽  
Chondroitin Sulphate ◽  
Chain Structure ◽  
Bioactive Molecules ◽  
Biological Information ◽  
Extracellular Milieu ◽  
Overwhelming Evidence ◽  
Chemical Messenger ◽  
Cellular Behaviour

Chondroitin sulphate (CS) glycosaminoglycan chains on cell and extracellular matrix proteoglycans (PGs) can no longer be regarded as merely hydrodynamic space fillers. Overwhelming evidence over recent years indicates that sulphation motif sequences within the CS chain structure are a source of significant biological information to cells and their surrounding environment. CS sulphation motifs have been shown to interact with a wide variety of bioactive molecules, e.g. cytokines, growth factors, chemokines, morphogenetic proteins, enzymes and enzyme inhibitors, as well as structural components within the extracellular milieu. They are therefore capable of modulating a panoply of signalling pathways, thus controlling diverse cellular behaviours including proliferation, differentiation, migration and matrix synthesis. Consequently, through these motifs, CS PGs play significant roles in the maintenance of tissue homeostasis, morphogenesis, development, growth and disease. Here, we review (i) the biodiversity of CS PGs and their sulphation motif sequences and (ii) the current understanding of the signalling roles they play in regulating cellular behaviour during tissue development, growth, disease and repair.

Honeycomb Lung: Time for a Change

2015 ◽  
Vol 139 (11) ◽  
pp. 1398-1399 ◽  
Author(s):  
Richard L. Kradin
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Lung Disease ◽  
Interstitial Pneumonia ◽  
Late Stage ◽  
Usual Interstitial Pneumonia ◽  
Biological Information ◽  
Pulmonary Acinus ◽  
End Stage ◽  
Dying Back

The recent introduction of new US Food and Drug Administration–approved medications for the treatment of idiopathic pulmonary fibrosis/usual interstitial pneumonia raises important concerns about the accuracy of diagnosis. The term honeycomb lung, used widely by radiologists and pathologists in the diagnosis of usual interstitial pneumonia, represents a late stage of the disease and conveys no biological information. A new conception of end-stage lung disease in usual interstitial pneumonia, based on the dying back of the pulmonary acinus, is proposed, which may improve the sensitivity and specificity of the diagnosis and provide an understanding of its pathogenesis.

scholarly journals Hyponatremia – unfavourable prognostic factor in hepatic cirrhosis

2016 ◽  
Vol 54 (4) ◽  
pp. 207-210
Author(s):  
Aurelia Enescu ◽  
F. Petrescu ◽  
P. Mitruţ ◽  
V. Pădureanu ◽  
Octavia Ileana Petrescu ◽  
...  
Keyword(s):  
Hepatic Cirrhosis ◽  
Signs And Symptoms ◽  
Hepatic Disease ◽  
Definitive Treatment ◽  
Brain Cells ◽  
Hepatic Diseases ◽  
The Central Nervous System ◽  
End Stage ◽  
The Brain ◽  
Unfavourable Prognostic Factor

Abstract Hyponatremia is defined by a level of Na in serum below or equal to 136 mEq/L while in hepatic cirrhosis it is classically considered as relevant only at a level of Na below 130 mEq/L. Hyponatremia frequently occurs in patients with end-stage hepatic disease. The frequency and severity are variable but it has been estimated that it occurs with a frequency of 57% in hospitalized patients with cirrhosis and in those on waiting lists for hepatic transplants. Signs and symptoms of hyponatremia are related to dysfunctions of the central nervous system, due to migration of the water from intravascular space to the brain cells, resulting in the occurrence of cerebral edema. Therapeutic options in hyponatremia are limited and are based on restriction of water consumption, exclusion of diuretics and vaptans. Hepatic transplant remains the only definitive treatment for end-stage hepatic diseases in which hyponatremia has occurred.

scholarly journals Inflammatory Cytokine Profile and Plasticity of Brain and Spinal Microglia in Response to ATP and Glutamate

2021 ◽  
Vol 15 ◽  
Author(s):  
Sam Joshva Baskar Jesudasan ◽  
Somnath J. Gupta ◽  
Matthew A. Churchward ◽  
Kathryn G. Todd ◽  
Ian R. Winship
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
Inflammatory Factors ◽  
Surrounding Environment ◽  
Glial Cultures ◽  
Inflammatory Phenotype ◽  
The Central Nervous System ◽  
Molecular Patterns

Microglia are the primary cells in the central nervous system that identify and respond to injury or damage. Such a perturbation in the nervous system induces the release of molecules including ATP and glutamate that act as damage-associated molecular patterns (DAMPs). DAMPs are detected by microglia, which then regulate the inflammatory response in a manner sensitive to their surrounding environment. The available data indicates that ATP and glutamate can induce the release of pro inflammatory factors TNF (tumor necrosis factor), IL-1β (interleukin 1 beta), and NO (nitric oxide) from microglia. However, non-physiological concentrations of ATP and glutamate were often used to derive these insights. Here, we have compared the response of spinal cord microglia (SM) relative to brain microglia (BM) using physiologically relevant concentrations of glutamate and ATP that mimic injured conditions in the central nervous system. The data show that ATP and glutamate are not significant modulators of the release of cytokines from either BM or SM. Consistent with previous studies, spinal microglia exhibited a general trend toward reduced release of inflammatory cytokines relative to brain-derived microglia. Moreover, we demonstrate that the responses of microglia to these DAMPs can be altered by modifying the biochemical milieu in their surrounding environment. Preconditioning brain derived microglia with media from spinal cord derived mixed glial cultures shifted their release of IL-1ß and IL-6 to a less inflammatory phenotype consistent with spinal microglia.

scholarly journals The Banach-Tarski Paradox Dictates Snyergistic Routes for Scale-Free Neurodynamics

2020 ◽  
Author(s):  
Arturo Tozzi ◽  
James F. Peters
Keyword(s):  
Information Transfer ◽  
Neural Dynamics ◽  
Free Oscillations ◽  
Scale Invariant ◽  
Brain Areas ◽  
Scale Free ◽  
Cortical Oscillations ◽  
The Central Nervous System ◽  
Self Similar ◽  
Physical Changes

Neuroscientists are able to detect physical changes in information entropy in available neurodata. However, the information paradigm is inadequate to fully describe nervous dynamics and mental activities such as perception. This paper provides an effort to build explanations to neural dynamics alternative to thermodynamic and information accounts. We recall the Banach–Tarski paradox (BTP), which informally states that, when pieces of a ball are moved and rotated without changing their shape, a synergy between two balls of the same volume is achieved instead of the original one. We show how and why BTP might display this physical and biological synergy meaningfully, making it possible to tackle nervous activities. The anatomical and functional structure of the central nervous system’s nodes and edges allows to perform a sequence of moves inside the connectome that doubles the amount of available cortical oscillations. In particular, a BTP-based mechanism permits scale-invariant nervous oscillations to amplify and propagate towards far apart brain areas. Paraphrasing the BPT’s definition, we could state that: when a few components of a self-similar nervous oscillation are moved and rotated throughout the cortical connectome, two self-similar oscillations are achieved instead of the original one. Furthermore, based on topological structures, we illustrate how, counterintuitively, the amplification of scale-free oscillations does not require information transfer.

scholarly journals Inflammatory cytokine profile and plasticity of brain and spinal microglia in response to ATP and glutamate

2020 ◽  
Author(s):  
Sam Joshva Baskar Jesudasan ◽  
Somnath J Gupta ◽  
Matthew A Churchward ◽  
Kathryn Todd ◽  
Ian R Winship
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
Inflammatory Factors ◽  
Surrounding Environment ◽  
Glial Cultures ◽  
Inflammatory Phenotype ◽  
The Central Nervous System ◽  
Molecular Patterns

AbstractMicroglia are the primary cells in the central nervous system that identify and respond to injury or damage. Such a perturbation in the nervous system induces the release of molecules including ATP and glutamate that act as damage-associated molecular patterns (DAMPs). DAMPs are detected by microglia, which then regulate the inflammatory response in a manner sensitive to their surrounding environment. The available data indicates that ATP and glutamate can induce the release of pro inflammatory factors TNF (tumor necrosis factor), IL-1β (interleukin 1 beta) and NO (nitric oxide) from microglia. However, non-physiological concentrations of ATP and glutamate were often used to derive these insights. Here, we have compared the response of spinal cord microglia (SM) relative to brain microglia (BM) using physiologically relevant concentrations of glutamate and ATP that mimic injured conditions in the central nervous system. The data show that ATP and glutamate are not significant modulators of the release of cytokines from either BM or SM. Consistent with previous studies, spinal microglia exhibited a general trend towards reduced release of inflammatory cytokines relative to brain-derived microglia. Moreover, we demonstrate that the responses of microglia to these DAMPs can be altered by modifying the biochemical milieu in their surrounding environment. Preconditioning brain derived microglia with media from spinal cord derived mixed glial cultures shifted their release of IL-ß, IL-6 and IL-10 to a less inflammatory phenotype consistent with a spinal microglia.

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