Growth requirements in vitro of oligodendrocyte cell lines and neonatal rat brain oligodendrocytes.

Bottenstein, Jane E.

doi:10.1073/pnas.83.6.1955

Cited by 100 publications

(80 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Primary cultures of mouse brain neural cells were obtained as described (17,18). BALB/c mouse brains were dissociated in an isotonic buffer (19) containing 0.25% trypsin and 0.001% DNase I.…”

Section: Methodsmentioning

confidence: 99%

Osteopetrosis and thalamic hypomyelinosis with synaptic degeneration in DAP12-deficient mice

Kaifu¹,

Nakahara²,

Inui³

et al. 2003

J. Clin. Invest.

303

247

View full text Add to dashboard Cite

Section: Methodsmentioning

confidence: 99%

Osteopetrosis and thalamic hypomyelinosis with synaptic degeneration in DAP12-deficient mice

Kaifu¹,

Nakahara²,

Inui³

et al. 2003

J. Clin. Invest.

303

247

View full text Add to dashboard Cite

“…SEPP1 is required to maintain normal selenium levels in several tissues, including the CNS (Hill et al, 2003), and deficiencies in SEPP1 lead to neurological defects (Schweizer et al, 2004). Although selenium and SEPP1 have been found to be strongly neurotrophic (Yan and Barrett, 1998), these effects may also partially be mediated by disruptions in normal OL development: selenium is required for the survival and differentiation of oligodendrocyte lineage cells in vitro (Bottenstein, 1986), and for myelin gene upregulation (Gu et al, 1997). In addition, there have been suggestions that environmental deficits in selenium could be a contributing risk factor for MS (Hasanen et al, 1986;Irvine et al, 1989) and that selenium supplementation might be beneficial (Clausen et al, 1988).…”

Section: Identification Of New Candidate Genes That May Govern Ms Susmentioning

confidence: 99%

Functional Genomic Analysis of Oligodendrocyte Differentiation

Dugas¹,

Tai²,

Speed³

et al. 2006

J. Neurosci.

294

353

View full text Add to dashboard Cite

To better understand the molecular mechanisms governing oligodendrocyte (OL) differentiation, we have used gene profiling to quantitatively analyze gene expression in synchronously differentiating OLs generated from pure oligodendrocyte precursor cells in vitro. By comparing gene expression in these OLs to OLs generated in vivo, we discovered that the program of OL differentiation can progress normally in the absence of heterologous cell-cell interactions. In addition, we found that OL differentiation was unexpectedly prolonged and occurred in at least two sequential stages, each characterized by changes in distinct complements of transcription factors and myelin proteins. By disrupting the normal dynamic expression patterns of transcription factors regulated during OL differentiation, we demonstrated that these sequential stages of gene expression can be independently controlled. We also uncovered several genes previously uncharacterized in OLs that encode transmembrane, secreted, and cytoskeletal proteins that are as highly upregulated as myelin genes during OL differentiation. Last, by comparing genomic loci associated with inherited increased risk of multiple sclerosis (MS) to genes regulated during OL differentiation, we identified several new positional candidate genes that may contribute to MS susceptibility. These findings reveal a previously unexpected complexity to OL differentiation and suggest that an intrinsic program governs successive phases of OL differentiation as these cells extend and align their processes, ensheathe, and ultimately myelinate axons.

show abstract

“…Methods to selectively enrich for type 2 astrocytes generally include size-based exclusion techniques (Juurlink and Hertz, 1991), immunopanning (Foo et al, 2011;Cahoy et al, 2008), and different tissue culture media formulations compared to those used to grow type 1 astrocytes (Juurlink and Hertz, 1991) (Table 1.2). (Chen et al, 2007, Bottenstein, 1986, Besnard et al, 1989 Yes No…”

Section: Culturing Glial Cellsmentioning

confidence: 99%

“…Fibroblast growth factor (FGF) (Bottenstein, 1986, Besnard et al, 1989, Chen et al, 2007 Yes No 3,3′,5-Triiodo-L-thyronine (Knapp et al, 1987) Yes No de Vellis, 1980, Bottenstein, 1986) <5% 10%…”

Section: Biotinmentioning

confidence: 99%

See 1 more Smart Citation

Development of a simple in vitro mature mixed glial model to investigate differential expression of cell markers on glial cells and their potential as targets in multiple sclerosis

Beasley¹

View full text Add to dashboard Cite

Autoantibodies are present in many patients with demyelinating diseases and have been shown to have pathogenic potential in the case of people with neuromyelitis optica (NMO). However, it is still debated whether antibodies that are present in people with multiple sclerosis (MS) are pathogenic. There are multiple different mechanisms by which autoantibodies could exert their effects in MS, and they could potentially target any cell/structure within the central nervous system (CNS), although the focus of antibody studies in MS has been almost solely on myelin antigens. Recently, however, some evidence has suggested that astrocytes could also be targeted in MS. Therefore, there is a need for a simple but robust in vitro model to allow the testing of antibodies against oligodendrocytes and astrocytes. The hypothesis tested in this thesis is that a cell culture model containing a mixture of mature glial cells could be a useful model by which to test the pathogenicity of the antibodies from people with MS, and the antigens that they are targeting. In order to test this hypothesis, this thesis set out to develop a mature mixed glial cell culture model, to test whether one cell type could be killed without impacting on the health of the other cells, and to then use this model to test antibodies from people with MS.Chapter 2 describes the development of a rat neonatal-derived mature mixed glial culture. A method was developed that allowed cultures with a mixture of protoplasmic (type 1) and fibrous (type 2) astrocytes to grow alongside mature oligodendrocytes. This method did not rely on addition of extra growth factors, presumably due to the production of all factors required for growth of each cell type by the other cells in the mixed culture. Because of this co-dependence on the other cells in the mixed culture for growth and development, the next step was to test whether specific targeting (killing) of one cell would result in the death of the other cells in culture, as that could potentially interfere with the interpretation of results in later chapters investigating the effects of antibodies in patient sera. In Chapter 3, it was found that oligodendrocytes could be selectively targeted (using a commercially-available antibody against sulfatide) and the astrocytes remained unaffected. It proved to be more difficult to find a cell surface-expressed molecule that could target only astrocytes and not have ii adverse effects on oligodendrocytes. In the literature, one molecule that is generally considered to be expressed on astrocytes, but not oligodendrocytes, is GLAST, a glutamate transporter. Initial studies using an antibody against the intracellular N-terminus of GLAST confirmed that only astrocytes in culture were stained by this antibody. An antibody was therefore generated that was specific for an epitope of GLAST ) that is expressed on the extracellular side of the membrane. However, when this antibody was tested for its ability to kill astrocytes in culture, both oligodendrocytes and astrocytes were ...

show abstract

Growth requirements in vitro of oligodendrocyte cell lines and neonatal rat brain oligodendrocytes.

Cited by 100 publications

References 34 publications

Osteopetrosis and thalamic hypomyelinosis with synaptic degeneration in DAP12-deficient mice

Osteopetrosis and thalamic hypomyelinosis with synaptic degeneration in DAP12-deficient mice

Functional Genomic Analysis of Oligodendrocyte Differentiation

Development of a simple in vitro mature mixed glial model to investigate differential expression of cell markers on glial cells and their potential as targets in multiple sclerosis

Contact Info

Product

Resources

About