Differentiation of Serum-Free Mouse Embryo Cells into an Astrocytic Lineage is Associated with the Asymmetric Production of Early Neural, Neuronal and Glial Markers

Yamaguchi, Hideaki; Kidachi, Yumi; Umetsu, Hironori; Ryoyama, Kazuo

doi:10.1248/bpb.31.1008

Cited by 3 publications

(2 citation statements)

References 61 publications

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“…For F-actin labeling, cells were incubated with rhodamine-phalloidin. As previously reported, 12) the anti-bIII-tubulin antibody in the present study showed appropriate specificities (data not shown). For bIIItubulin labeling, cells were blocked in Tris-buffered saline containing 0.05% Tween-20 and 3% non-fat dried milk.…”

Section: Methodssupporting

confidence: 90%

Glycyrrhetinic Acid Induces Anoikis-Like Death and Cytoskeletal Disruption in the Central Nervous System Tumorigenic Cells

Yamaguchi

Kidachi

Kamiie

et al. 2010

Biological & Pharmaceutical Bulletin

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Licorice extracts and the principal licorice component glycyrrhizin (GL) are used worldwide in foods, tobacco and medicines. The sweet taste of licorice roots arises from GL, which is reputed to be at least 50 times sweeter than refined sugar. Owing to this sweetness, GL is extensively used as a natural sweetener and flavoring additive.1) GL is a saponin compound comprising a triterpenoid aglycone, glycyrrhetinic acid (GA), conjugated to a disaccharide of glucuronic acid. GA is used as an antitoxic and immunological regulatory agent for the prevention or treatment of viral infection, inflammation and anaphylaxis.2,3) However, despite its wide use in the market and great effects on some physiological aspects, to the best of our knowledge, no studies have investigated the antitumor effects of GA on tumor cells in the central nervous system (CNS).Serum-free mouse embryo (SFME) cells were originally derived from a 16-d-old whole Balb/c mouse embryo and are maintained in a serum-free culture medium.4) These cells do not undergo growth crisis, maintain their diploid karyotype for extended passages and are non-tumorigenic in vivo. Consequently, they are non-transformed, behave as primary cultures, have a finite lifespan and display the characteristics of CNS progenitor cells.5,6) SFME cells were cotransfected with the human c-Ha-ras and mouse c-myc genes, and the resulting cells were designated ras/myc SFME cells. 7) While SFME cells are non-tumorigenic in vivo, 5,6) ras/myc SFME cells are tumorigenic and do not require any growth factors, such as epidermal growth factor. 7) Another line of SFME-derived tumorigenic cells are highly metastatic ras/myc SFME-1 (r/m HM-SFME-1) cells, which were established by selecting ras/myc SFME cells that only metastasize to the lungs of Balb/c mice. 8) In the present study, r/m HM-SFME-1 cells were treated with GA and its efficacy as an antitumor agent through anoikis-like cell death and cytoskeletal disruption was investigated. Cell Culture SFME and r/m HM-SFME-1 cells were cultured in a humidified 5% CO 2 -95% air atmosphere at 37°C in 60 mm diameter dishes, pre-coated with 10 mg/ml fibronectin. The basal nutrient culture medium was a 1 : 1 mixture of Dulbecco's modified Eagle's medium and Ham's F12 9,10) containing 15 mM N-(2-hydroxyethyl)piperazine-NЈ-2-ethanesulfonic acid (HEPES), pH 7.4, 1.2 mg/ml sodium bicarbonate, 10 nM sodium selenite and 10 mg/ml gentamicin, supplemented with insulin (10 mg/ml), transferrin (25 mg/ml) and epidermal growth factor (50 ng/ml). Cell passages were accomplished by rapid trypsinization with 0.2% crude trypsin and 1 mM ethylenediaminetetraacetate in phosphatebuffered saline (PBS) without calcium or magnesium, followed by dilution in the culture medium at room temperature. The medium containing the collected cells was centrifuged at 250 g at 4°C for 7 min and the supernatant was removed. The cells were suspended in the culture medium without the supplements, plated at 1ϫ10 5 cells/dish and cultured again in the medium with the supplements. Following...

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Section: Methodssupporting

confidence: 90%

Glycyrrhetinic Acid Induces Anoikis-Like Death and Cytoskeletal Disruption in the Central Nervous System Tumorigenic Cells

Yamaguchi

Kidachi

Kamiie

et al. 2010

Biological & Pharmaceutical Bulletin

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“…Many reports show that astrocytes express ion channels, both ligand-gated and voltage-dependent [1], have the general functions of clearing neurotransmitters and ions away from the synapse [2, 3] and more direct and active roles in synapse function [4, 5]. There also are some reports showing that astrocytes play an important role in regulating the function of oligodendrocytes [6, 7] and neural stem cells [8, 9]. …”

Section: Astrocyte and Astrogliosismentioning

confidence: 99%

Astrogliosis in CNS Pathologies: Is There A Role for Microglia?

et al. 2010

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Astrogliosis, a cellular reaction with specific structural and functional characteristics, represents a remarkably homotypic response of astrocytes to all kinds of central nervous system (CNS) pathologies. Astrocytes play diverse functions in the brain, both harmful and beneficial. Mounting evidence indicates that astrogliosis is an underlying component of a diverse range of diseases and associated neuropathologies. The mechanisms that lead to astrogliosis are not fully understood, nevertheless, damaged neurons have long been reported to induce astrogliosis and astrogliosis has been used as an index for underlying neuronal damage. As the predominant source of proinflammatory factors in the CNS, microglia are readily activated under certain pathological conditions. An increasing body of evidence suggests that release of cytokines and other soluble products by activated microglia can significantly influence the subsequent development of astrogliosis and scar formation in CNS. It is well known that damaged neurons activate microglia very quickly, therefore, it is possible that activated microglia contribute factors/mediators through which damaged neuron induce astrogliosis. The hypothesis that activated microglia initiate and maintain astrogliosis suggests that suppression of microglial overactivation might effectively attenuate reactive astrogliosis. Development of targeted anti-microglial activation therapies might slow or halt the progression of astrogliosis and, therefore, help achieve a more beneficial environment in various CNS pathologies.

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Toluene Abuse and White Matter Degeneration

Bigio

2016

Neuropathology of Drug Addictions and Substance Misuse

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Differentiation of Serum-Free Mouse Embryo Cells into an Astrocytic Lineage is Associated with the Asymmetric Production of Early Neural, Neuronal and Glial Markers

Cited by 3 publications

References 61 publications

Glycyrrhetinic Acid Induces Anoikis-Like Death and Cytoskeletal Disruption in the Central Nervous System Tumorigenic Cells

Glycyrrhetinic Acid Induces Anoikis-Like Death and Cytoskeletal Disruption in the Central Nervous System Tumorigenic Cells

Astrogliosis in CNS Pathologies: Is There A Role for Microglia?

Toluene Abuse and White Matter Degeneration

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