scholarly journals To Be or Not to Be: Environmental Factors that Drive Myelin Formation during Development and after CNS Trauma

Neuroglia ◽  
2018 ◽  
Vol 1 (1) ◽  
pp. 63-90 ◽  
Author(s):  
Nicole Pukos ◽  
Rim Yoseph ◽  
Dana M. McTigue

Oligodendrocytes are specialized glial cells that myelinate central nervous system (CNS) axons. Historically, it was believed that the primary role of myelin was to compactly ensheath axons, providing the insulation necessary for rapid signal conduction. However, mounting evidence demonstrates the dynamic importance of myelin and oligodendrocytes, including providing metabolic support to neurons and regulating axon protein distribution. As such, the development and maintenance of oligodendrocytes and myelin are integral to preserving CNS homeostasis and supporting proper functioning of widespread neural networks. Environmental signals are critical for proper oligodendrocyte lineage cell progression and their capacity to form functional compact myelin; these signals are markedly disturbed by injury to the CNS, which may compromise endogenous myelin repair capabilities. This review outlines some key environmental factors that drive myelin formation during development and compares that to the primary factors that define a CNS injury milieu. We aim to identify developmental factors disrupted after CNS trauma as well as pathogenic factors that negatively impact oligodendrocyte lineage cells, as these are potential therapeutic targets to promote myelin repair after injury or disease.

2014 ◽  
Vol 34 (3) ◽  
pp. 369-375 ◽  
Author(s):  
Juan Pablo de Rivero Vaccari ◽  
W Dalton Dietrich ◽  
Robert W Keane

The inflammasome is an intracellular multiprotein complex involved in the activation of caspase-1 and the processing of the proinflammatory cytokines interleukin-1 β (IL-1 β) and IL-18. The inflammasome in the central nervous system (CNS) is involved in the generation of an innate immune inflammatory response through IL-1 cytokine release and in cell death through the process of pyroptosis. In this review, we consider the different types of inflammasomes (NLRP1, NLRP2, NLRP3, and AIM2) that have been described in CNS cells, namely neurons, astrocytes, and microglia. Importantly, we focus on the role of the inflammasome after brain and spinal cord injury and cover the potential activators of the inflammasome after CNS injury such as adenosine triphosphate and DNA, and the therapeutic potential of targeting the inflammasome to improve outcomes after CNS trauma.


Author(s):  
Lisa-ann Gershwin

While it is generally assumed that jellyfishes (Cnidaria: Scyphozoa) are stably tetramerous, variation in symmetry (i.e. unimerous to octamerous) can be observed in most populations at a rate of approximately 2%, but sometimes as high as 10%. This type of variation has been observed among clonemates during strobilation in five taxa, namely Aurelia aurita, A. labiata, Chrysaora fuscescens, Pelagia colorata, and Phacellophora camtschatica. It is currently unclear whether the symmetry variation is caused by genetic, environmental, or developmental factors, or some combination. Although hexamerous lineages were not bred successfully, lineages were raised with rates of variation higher than normal. Thus, there may be some genetic component to the variation. In one lineage observed over 4.5 months, the rate of non-tetramery declined substantially from an initial high of 88.9% to a final cumulative low of 29%. Apparently this lineage was able to stabilize tetramery over time, possibly indicating some self-correcting developmental mechanism. Furthermore, no difference was found in variation rates between stressed and unstressed polyps, indicating that environmental factors may not play an important role in symmetry determination in these animals. These results indicate stabilizing selection in controlling the expression of variable symmetry.


2018 ◽  
Vol 19 (11) ◽  
pp. 3425 ◽  
Author(s):  
Céline Tiffon

Environmental epigenetics describes how environmental factors affect cellular epigenetics and, hence, human health. Epigenetic marks alter the spatial conformation of chromatin to regulate gene expression. Environmental factors with epigenetic effects include behaviors, nutrition, and chemicals and industrial pollutants. Epigenetic mechanisms are also implicated during development in utero and at the cellular level, so environmental exposures may harm the fetus by impairing the epigenome of the developing organism to modify disease risk later in life. By contrast, bioactive food components may trigger protective epigenetic modifications throughout life, with early life nutrition being particularly important. Beyond their genetics, the overall health status of an individual may be regarded as an integration of many environmental signals starting at gestation and acting through epigenetic modifications. This review explores how the environment affects the epigenome in health and disease, with a particular focus on cancer. Understanding the molecular effects of behavior, nutrients, and pollutants might be relevant for developing preventative strategies and personalized heath programs. Furthermore, by restoring cellular differentiation, epigenetic drugs could represent a potential strategy for the treatment of many diseases including cancer.


2013 ◽  
Vol 06 (03) ◽  
pp. 089-093
Author(s):  
Rita P. Raman ◽  
Anita D. Raman

ABSTRACTThe specific genetic alterations that result in diseases and complex syndromes have been and continue to be identified. Search for the origins of disease have led to investigations into the roles of dietary and environmental factors as potential triggers or modifiers of risk. Genome-wide association studies have identified concepts such as the rare variant-common disease hypothesis and the common variant-common disease hypothesis.1 Through association studies, unique gene-environment interactions, which may occur with or without specific periods of permissiveness or vulnerabilities, have also been identified. Major conditions where the role of exposomes and epigenetics are rapidly evolving are obesity, neurological disorders, immune disorders and cancers. These concepts are particularly intriguing in the context of obesity. BACKGROUND: Epigenetics can be defined as heritable traits resulting from changes in DNA or chromatin structure without alterations in the DNA sequence.2 Nutritional epigenetics is seen as a means for the prevention of developmental diseases and cancer, and to delay processes associated with aging.3,4 Diseases in which epigenetic factors are considered significant include type 2 diabetes mellitus, obesity, inflammation, cardiovascular diseases, neurocognitive disorders, and immune diseases, with neural function influenced by environmental factors including early experience.5 Studies with rodent models suggest that during both early development and in adult life, environmental signals can activate intracellular pathways that directly remodel the epigenome, leading to changes in gene expression and function. These studies define a biological basis for the interplay between environmental signals and the genome in the regulation of individual differences in behavior, cognition, and physiology.6 In reproduction, certain genes are turned on while others are turned off in the process of imprinting. In the case of imprinting, even though there are two copies of the gene, only one copy is expressed and there is no substitute functional allele. For this reason, imprinting makes the imprinted genes more vulnerable to the negative effects of mutations.7


2021 ◽  
Vol 22 (2) ◽  
pp. 765
Author(s):  
Gaojie Li ◽  
Shiqi Hu ◽  
Xuyao Zhao ◽  
Sunjeet Kumar ◽  
Yixian Li ◽  
...  

Plants adapt to environmental changes by regulating their development and growth. As an important interface between plants and their environment, leaf morphogenesis varies between species, populations, or even shows plasticity within individuals. Leaf growth is dependent on many environmental factors, such as light, temperature, and submergence. Phytohormones play key functions in leaf development and can act as molecular regulatory elements in response to environmental signals. In this review, we discuss the current knowledge on the effects of different environmental factors and phytohormone pathways on morphological plasticity and intend to summarize the advances in leaf development. In addition, we detail the molecular mechanisms of heterophylly, the representative of leaf plasticity, providing novel insights into phytohormones and the environmental adaptation in plants.


2020 ◽  
Vol 21 (17) ◽  
pp. 6155
Author(s):  
Jae Sung Shim ◽  
Geupil Jang

The transition from the vegetative to the reproductive stage of growth is a critical event in the lifecycle of a plant and is required for the plant’s reproductive success. Flowering time is tightly regulated by an internal time-keeping system and external light conditions, including photoperiod, light quality, and light quantity. Other environmental factors, such as drought and temperature, also participate in the regulation of flowering time. Thus, flexibility in flowering time in response to environmental factors is required for the successful adaptation of plants to the environment. In this review, we summarize our current understanding of the molecular mechanisms by which internal and environmental signals are integrated to regulate flowering time in Arabidopsis thaliana and rice (Oryza sativa).


2009 ◽  
Vol 191 (17) ◽  
pp. 5358-5368 ◽  
Author(s):  
Prahathees Eswaramoorthy ◽  
Tao Guo ◽  
Masaya Fujita

ABSTRACT Sensor histidine kinases are widely used by bacteria to detect and respond to environmental signals. In Bacillus subtilis, KinA is a major kinase providing phosphate input to the phosphorelay that activates the sporulation pathway upon starvation via the phosphorylated Spo0A transcription factor. KinA contains three PAS domains in its amino-terminal sensor domain, which appear to be involved in the sensing of an unidentified sporulation signal(s) produced upon starvation. Prior biochemical studies have suggested that KinA forms a homodimer as a functional enzyme and that the most amino-terminal PAS domain (PAS-A) plays an important role in sensing the signal(s) to activate an ATP-dependent autophosphorylation reaction to a histidine residue. To analyze the structure and function of the kinase in vivo, we have used a strain in which the synthesis of KinA is under the control of an isopropyl-β-d-thiogalactopyranoside (IPTG)-inducible promoter. In vivo functional studies in combination with domain-based deletion analysis show that the cytosolic KinA forms a homo-oligomer as an active form under both nutrient-rich and nutrient-depleted conditions via its amino- and carboxyl-terminal domains independently. Furthermore, we found that a mutant in which the PAS-A domain was deleted was still able to induce sporulation at a wild-type level irrespective of nutrient availability, suggesting that PAS-BC domains are sufficient to maintain the kinase activity. Based on these results, we propose that the primary role of the amino-terminal sensor domain is to form a stable complex as a functional kinase, but possibly not for the binding of an unidentified sporulation signal(s).


2017 ◽  
Vol 25 (1) ◽  
pp. 8-21 ◽  
Author(s):  
Mitchell T. Caprelli ◽  
Andrea J. Mothe ◽  
Charles H. Tator

The ideal biomarker for central nervous system (CNS) trauma in patients would be a molecular marker specific for injured nervous tissue that would provide a consistent and reliable assessment of the presence and severity of injury and the prognosis for recovery. One candidate biomarker is the protein tau, a microtubule-associated protein abundant in the axonal compartment of CNS neurons. Following axonal injury, tau becomes modified primarily by hyperphosphorylation of its various amino acid residues and cleavage into smaller fragments. These posttrauma products can leak into the cerebrospinal fluid or bloodstream and become candidate biomarkers of CNS injury. This review examines the primary molecular changes that tau undergoes following traumatic brain injury and spinal cord injury, and reviews the current literature in traumatic CNS biomarker research with a focus on the potential for hyperphosphorylated and cleaved tau as sensitive biomarkers of injury.


Author(s):  
Richard D. Newcomb ◽  
Richard J. Vetter ◽  
Clayton T. Cowl

Environmental medicine is the broad discipline that focuses on environmental factors that cause or influence disease. These factors typically are components of 4 major categories: air, water, soil, and food. Often, an environmental toxin or agent may have numerous means by which it causes disease, such as a toxin primarily soil bound that is aerosolized as dust or is made soluble and then infiltrates water and plants. The primary role of the clinician in environmental medicine is as a resource and risk communicator for patients. In circumstances where a patient has adverse health effects, the clinician's role is to determine how likely it is that an environmental toxin has contributed to the patient's symptoms or an underlying disease. When a hazard is recognized, the clinician helps control and reduce exposure, as well as treats any illness when effective treatment options are available.


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