Markers for OLN-93 oligodendroglia differentiation

Meeteren, M.E. van; Koetsier, Marleen A.; Dijkstra, Christine D.; Tol, Eric A.F. van

doi:10.1016/j.devbrainres.2005.02.005

Cited by 10 publications

(11 citation statements)

References 38 publications

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“…At the protein level, OLN-93 cells do not express MOG or the astrocytic marker GFAP, although mRNAs for these proteins and also for PLP could be detected. This contrasts the study of van Meeteren et al (2005) who stated that even PLP and MOG mRNA expression were very weak or undetectable in samples of OLN-93 cells after differentiation in serum-free medium supplemented with insulin-like growth factor-I (IGF-I). This addition of IGF-I could explain the discrepancy with our results.…”

Section: Serum-deprived Oln-93 Cells Undergo Drastic Morphological Chcontrasting

confidence: 56%

Morphological changes do not reflect biochemical and functional differentiation in OLN-93 oligodendroglial cells

Buckinx

Smolders

Sahebali

et al. 2009

Journal of Neuroscience Methods

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Section: Serum-deprived Oln-93 Cells Undergo Drastic Morphological Chcontrasting

confidence: 56%

Morphological changes do not reflect biochemical and functional differentiation in OLN-93 oligodendroglial cells

Buckinx

Smolders

Sahebali

et al. 2009

Journal of Neuroscience Methods

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“…Discrepancy in the observed metabolic activity of cells when tested for cell viability and cell proliferation may be linked to different serum concentration in the incubation medium, reduced (2 %) or standard (10 %), respectively. According to several studies describing intracellular modifications in OLN-93 cells in low-serum and serum-deprivation conditions [6, 7, 9] we cannot exclude the influence of various culture conditions on our study results. However, taking into consideration described measurements as well as microscopic observations of KYNA treated OLN-93 cells, we may clearly conclude that KYNA (1–1000 µM) does not affect OLN-93 cells proliferation, DNA synthesis and morphology, yet in concentration range 250–1000 µM it downregulates viability/metabolic activity of oligodendrocytes grown in a medium with a reduced serum concentration.…”

Section: Discussionmentioning

confidence: 96%

Kynurenic Acid Induces Impairment of Oligodendrocyte Viability: On the Role of Glutamatergic Mechanisms

et al. 2016

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Kynurenic acid (KYNA) is an end stage product of tryptophan metabolism with a variety of functions in the human body, both in the central nervous system (CNS) and in other organs. Although its activity in the human brain has been widely studied and effects on neural cells were emphasized, the effect of KYNA on oligodendroglial cells remains unknown. Present study aims at describing the activity of high concentration of KYNA in OLN-93 cells. The inhibition of OLN-93 oligodendrocytes viability by KYNA in a medium with reduced serum concentration has been demonstrated. Although decreased metabolic activity of KYNA treated OLN-93 cells was shown, the cells proliferation was not altered. KYNA treatment did not alter morphology as well as expression level of cell cycle and proliferation regulating proteins. Furthermore, glutamate receptor antagonists and agonists did not alter the inhibitory effect of KYNA on viability of OLN-93 oligodendrocytes. This study contributes to the elucidation of effects of KYNA on oligodendrocytes in vitro, yet further analyses are necessary to explain the mechanisms behind the damage and loss of myelin sheaths.

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“…After the 48‐hr period, the cells start to lose the fully developed, arborized morphology and eventually die. The cell line allows fast and easy cultivation and has been used in many studies as a model for OLGs (Richter‐Landsberg and Heinrich, 1996; Lee et al, 2005; van Meeteren et al, 2005).…”

Section: Methodsmentioning

confidence: 99%

Simvastatin interferes with process outgrowth and branching of oligodendrocytes

Smolders

Smets

Maier

et al. 2010

J of Neuroscience Research

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Statins have attracted interest as a treatment option for multiple sclerosis (MS) because of their pleiotropic antiinflammatory and immunomodulatory effects. However, contradictory results have been described when they are applied to oligodendrocytes (OLGs), the cell type predominantly affected in MS. In this study we focus on the in vitro effect of statins on process outgrowth in OLN-93 cells, a well-characterized OLG-derived cell line, and primary cultures of neonatal rat OLGs. Application of the lipophilic simvastatin, as low as 0.1-1 μM, disturbs process formation of both cell types, leading to less ramified cells. We show that both protein isoprenylation and cholesterol synthesis are required for the normal differentiation of OLGs. It is further demonstrated that the expression of 2',3'-cyclic-nucleotide-3' phosphodiesterase (CNP) and tubulin is lowered, concomitant with a reduction of membrane-bound CNP as well as tubulin. Therefore, we propose that lack of isoprenylation of CNP could help to explain the altered morphological and biochemical differentiation state of treated OLGs. Moreover, expression of specific myelin markers, such as myelin basic protein, myelin-associated glycoprotein, and myelin oligodendrocyte glycoprotein, was compromised after treatment. We conclude that simvastatin treatment has detrimental effects on OLG process outgrowth, the prior step in (re)myelination, thereby mortgaging long-term healing of MS lesions.

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Markers for OLN-93 oligodendroglia differentiation

Cited by 10 publications

References 38 publications

Morphological changes do not reflect biochemical and functional differentiation in OLN-93 oligodendroglial cells

Morphological changes do not reflect biochemical and functional differentiation in OLN-93 oligodendroglial cells

Kynurenic Acid Induces Impairment of Oligodendrocyte Viability: On the Role of Glutamatergic Mechanisms

Simvastatin interferes with process outgrowth and branching of oligodendrocytes

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