17
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Elimination of the geomagnetic field stimulates the proliferation of mouse neural progenitor and stem cells

      research-article

      Read this article at

      ScienceOpenPublisherPMC
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Living organisms are exposed to the geomagnetic field (GMF) throughout their lifespan. Elimination of the GMF, resulting in a hypogeomagnetic field (HMF), leads to central nervous system dysfunction and abnormal development in animals. However, the cellular mechanisms underlying these effects have not been identified so far. Here, we show that exposure to an HMF (<200 nT), produced by a magnetic field shielding chamber, promotes the proliferation of neural progenitor/stem cells (NPCs/NSCs) from C57BL/6 mice. Following seven-day HMF-exposure, the primary neurospheres (NSs) were significantly larger in size, and twice more NPCs/NSCs were harvested from neonatal NSs, when compared to the GMF controls. The self-renewal capacity and multipotency of the NSs were maintained, as HMF-exposed NSs were positive for NSC markers (Nestin and Sox2), and could differentiate into neurons and astrocyte/glial cells and be passaged continuously. In addition, adult mice exposed to the HMF for one month were observed to have a greater number of proliferative cells in the subventricular zone. These findings indicate that continuous HMF-exposure increases the proliferation of NPCs/NSCs, in vitro and in vivo. HMF-disturbed NPCs/NSCs production probably affects brain development and function, which provides a novel clue for elucidating the cellular mechanisms of the bio-HMF response.

          Electronic supplementary material

          The online version of this article (doi:10.1007/s13238-016-0300-7) contains supplementary material, which is available to authorized users.

          Related collections

          Most cited references58

          • Record: found
          • Abstract: found
          • Article: not found

          Stem cell aging: mechanisms, regulators and therapeutic opportunities.

          Aging tissues experience a progressive decline in homeostatic and regenerative capacities, which has been attributed to degenerative changes in tissue-specific stem cells, stem cell niches and systemic cues that regulate stem cell activity. Understanding the molecular pathways involved in this age-dependent deterioration of stem cell function will be critical for developing new therapies for diseases of aging that target the specific causes of age-related functional decline. Here we explore key molecular pathways that are commonly perturbed as tissues and stem cells age and degenerate. We further consider experimental evidence both supporting and refuting the notion that modulation of these pathways per se can reverse aging phenotypes. Finally, we ask whether stem cell aging establishes an epigenetic 'memory' that is indelibly written or one that can be reset.
            • Record: found
            • Abstract: found
            • Article: not found

            Strategies for homeostatic stem cell self-renewal in adult tissues.

            In adult tissues, an exquisite balance exists between stem cell proliferation and the generation of differentiated offspring. Classically, it has been argued that this balance is obtained at the level of a single stem cell, which divides strictly into a new stem cell and a progenitor. However, recent evidence suggests that balance can also be achieved at the level of the stem cell population. Some stem cells might be lost due to differentiation or damage, whereas others divide symmetrically to fill this gap. Here, we consider the general strategies for stem cell self-renewal and review the evidence for stochastic stem cell fate in adult tissues across a range of tissue types and organisms. Copyright © 2011 Elsevier Inc. All rights reserved.
              • Record: found
              • Abstract: found
              • Article: not found

              Physical exercise-induced hippocampal neurogenesis and antidepressant effects are mediated by the adipocyte hormone adiponectin.

              Adiponectin (ADN) is an adipocyte-secreted protein with insulin-sensitizing, antidiabetic, antiinflammatory, and antiatherogenic properties. Evidence is also accumulating that ADN has neuroprotective activities, yet the underlying mechanism remains elusive. Here we show that ADN could pass through the blood-brain barrier, and elevating its levels in the brain increased cell proliferation and decreased depression-like behaviors. ADN deficiency did not reduce the basal hippocampal neurogenesis or neuronal differentiation but diminished the effectiveness of exercise in increasing hippocampal neurogenesis. Furthermore, exercise-induced reduction in depression-like behaviors was abrogated in ADN-deficient mice, and this impairment in ADN-deficient mice was accompanied by defective running-induced phosphorylation of AMP-activated protein kinase (AMPK) in the hippocampal tissue. In vitro analyses indicated that ADN itself could increase cell proliferation of both hippocampal progenitor cells and Neuro2a neuroblastoma cells. The neurogenic effects of ADN were mediated by the ADN receptor 1 (ADNR1), because siRNA targeting ADNR1, but not ADNR2, inhibited the capacity of ADN to enhance cell proliferation. These data suggest that adiponectin may play a significant role in mediating the effects of exercise on hippocampal neurogenesis and depression, possibly by activation of the ADNR1/AMPK signaling pathways, and also raise the possibility that adiponectin and its agonists may represent a promising therapeutic treatment for depression.

                Author and article information

                Contributors
                yingliu@ibp.ac.cn
                herq@sun5.ibp.ac.cn
                Journal
                Protein Cell
                Protein Cell
                Protein & Cell
                Higher Education Press (Beijing )
                1674-800X
                1674-8018
                3 August 2016
                3 August 2016
                September 2016
                : 7
                : 9
                : 624-637
                Affiliations
                [1 ]State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101 China
                [2 ]Queensland Brain Institute, University of Queensland, Brisbane, QLD 4072 Australia
                [3 ]University of the Chinese Academy of Sciences, Beijing, 100049 China
                [4 ]Alzheimer’s Disease Center, Beijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069 China
                Author information
                http://orcid.org/0000-0002-1616-6916
                http://orcid.org/0000-0003-0802-3832
                Article
                300
                10.1007/s13238-016-0300-7
                5003790
                27484904
                b15bec21-0158-4752-a316-340a3e9b7bc7
                © The Author(s) 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 4 June 2016
                : 7 July 2016
                Categories
                Research Article
                Custom metadata
                © HEP and Springer 2016

                hypomagnetic field,neural progenitor/stem cells,neurosphere,proliferation,stemness,multipotency

                Comments

                Comment on this article

                Related Documents Log