Factors influencing astrocyte growth and development in defined media

Michler-Stuke, Angelika; Wolff, Joachim R.; Bottenstein, Jane E.

doi:10.1016/0736-5748(84)90035-2

Cited by 94 publications

(46 citation statements)

References 22 publications

(3 reference statements)

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“…After 1 week in culture, O2A progenitors, microglia, and residual neurons were removed by shaking overnight in an orbital shaker at 250 rpm. Cells were removed with trypsin and differentiated in defined medium containing the G5 supplement (Michler-Stuke et al, 1984) (Invitrogen, San Diego, CA). Cultures were 95% pure as determined by glial fibrillary acidic protein (GFAP) immunoreactivity.…”

Section: Methodsmentioning

confidence: 99%

Extracellular Heat Shock Protein 70: A Critical Component for Motoneuron Survival

Robinson¹,

Tidwell²,

Gould³

et al. 2005

J. Neurosci.

111

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The dependence of developing spinal motoneuron survival on a soluble factor(s) from their target, muscle tissue is well established both in vivo and in vitro. Considering this apparent dependence, we examined whether a specific component of the stress response mediates motoneuron survival in trophic factor-deprived environments. We demonstrate that, although endogenous expression of heat shock protein 70 (HSP70) did not change during trophic factor deprivation, application of e-rhHsp70 (exogenous recombinant human Hsp70) promoted motoneuron survival. Conversely, depletion of HSP70 from chick muscle extract (MEx) potently reduces the survivalpromoting activity of MEx. Additionally, exogenous treatment with or spinal cord overexpression of Hsp70 enhances motoneuron survival in vivo during the period of naturally occurring cell death [programmed cell death (PCD)]. Hindlimb muscle cells and lumbar spinal astrocytes readily secrete HSP70 in vitro, suggesting potential physiological sources of extracellular Hsp70 for motoneurons. However, in contrast to exogenous treatment with or overexpression of Hsp70 in vivo, muscle-targeted injections of this factor in an ex vivo preparation fail to attenuate motoneuron PCD. These data (1) suggest that motoneuron survival requirements may extend beyond classical trophic factors to include HSP70, (2) indicate that the source of this factor is instrumental in determining its trophic function, and (3) may therefore influence therapeutic strategies designed to increase motoneuron Hsp70 signaling during disease or injury.

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Section: Methodsmentioning

confidence: 99%

Extracellular Heat Shock Protein 70: A Critical Component for Motoneuron Survival

Robinson¹,

Tidwell²,

Gould³

et al. 2005

J. Neurosci.

111

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“…Thus, I have attempted to define the growth requirements of oligodendrocytes by using serum-free culture methods. The strategy of defining the requirements for growth of continuous cell lines expressing the phenotype of interest and applying this knowledge to culture of their normal cell counterparts has proven useful in the past for neurons and astrocytes (12)(13)(14)(15)(16)(17)(18)(19). Although these cell lines are of tumor origin, they share some of the growth requirements of their normal cell counterparts.…”

mentioning

confidence: 99%

“…16), and neonatal rat brain astrocytes (G5 medium; ref. 18). Cells were removed at confluence with 0.02% EGTA in PBS without Ca2l or Mg2", and any residual cells were hypotonically lysed.…”

mentioning

confidence: 99%

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

Bottenstein¹

1986

Proc. Natl. Acad. Sci. U.S.A.

100

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Growth requirements in vitro of oligodendrocyte cell lines and neonatal rat brain oligodendrocytes Branch, Galveston, TX 77550-2772 Communicated by Gordon H. Sato, November 15, 1985 ABSTRACT I have defined the basic requirements for the proliferation of cell lines expressing oligodendrocyte properties and for the survival of galactocerebroside-positive oligodendrocytes derived from neonatal rat brains. Conventional serum-containing medium can be replaced by 01 medium, a chemically defined medium supplemented with insulin, transferrin, sodium selenite, and biotin. Thyroid hormone is not required. When cells are plated directly into 01 medium, the substratum has to be modified by precoating with polylysine and adding fibronectin to the medium prior to the cells. Both cell lines and brain cells can be subcultured numerous times in 01 medium without initial culture in serum-containing medium. Brain cultures can be maintained in 01 medium for several months and contain a significantly higher percentage of mature oligodendrocytes, a lower number of astrocytes, and no fibroblasts as compared to cells maintained in serum-containing medium.

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“…When confluence was documented (days [12][13][14], the astrocytes were shaken at 400 rpm for 3 h to remove microglia and oligodendrocytes. Astrocytes were then maintained I day in G5 medium [15] to eliminate microglia and oligodendrocytes. Astrocyte cultures were characterized on the basis of morphologic criteria and by the expression of glial fibrillary acidic protein (GF AP) as detected by immunostaining.…”

Section: Fe3+ Plus U74389f V C H )mentioning

confidence: 99%

Protective Effect of a 21-Aminosteroid during Experimental Pneumococcal Meningitis

Lorenzi

Koedel

Frei

et al. 1995

Journal of Infectious Diseases

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This study investigated whether the 21-aminosteroid U74389F, an inhibitor of lipid peroxidation, attenuates pathophysiologic changes in experimental pneumococcal meningitis. Infected rats injected intravenously with vehicle and U74389F developed increases in regional cerebral blood flow (rCBF), intracranial pressure (ICP), brain water content, and white blood cells (WBC) in cerebrospinal fluid (CSF) within 8 h after intracisternal challenge. Pretreatment with or administration of U74389F 4 h after infection significantly reduced the increase in ICP but had no effect on rCBF increase. Moreover, U74389F pretreatment significantly reduced brain water content and CSF WBC count. In vitro, U74389F inhibited iron-dependent lipid peroxidation of astrocyte cultures and the production of tumor necrosis factor-a, interleukin-6, and nitric oxide by stimulated macrophages. These data suggest that U74389F modulates early pathophysiologic alterations in experimental pneumococcal meningitis.Animal models of bacterial meningitis have increased our knowledge of the complex pathophysiologic mechanisms of the disease [1][2][3][4][5]. In a rat model of meningitis, we showed that intracisternal (ic) inoculation of live pneumococci or pneumococcal cell wall components induces an early increase in regional cerebral blood flow (rCBF), intracranial pressure (lCP), and brain water content [6]. Pretreatment with free superoxide dismutase (SOD), polyethylene glycol (PEG)-conjugated SOD, deferoxamine, and catalase greatly attenuates these pathophysiologic changes; the strongest effects are shown with SOD and PEG-SOD [6][7][8]. Findings by other investigators support a role for reactive oxygen species in the pathophysiology of bacterial meningitis [9,10]. Cellular injury caused by reactive oxygen species may involve direct damage to proteins and DNA as well as lipid peroxidation [11]. Here we tested the effect of the novel 21-aminosteroid U74389F [12,13], an inhibitor of lipid peroxidation, for its capacity to alter rCBF, ICP, and brain edema formation and to reduce meningeal inflammation in experimental pneumococcal meningitis. Materials and MethodsAnimal preparation. We used a well-characterized rat meningitis model that has been described in detail [6]. Adult male Wistar rats (250-330 g) were intraperitoneally anesthetized with 100 mg! kg thiobutabarbiturate (lnactin; Byk Gulden, Konstanz, Germany), tracheotomized, and artificially ventilated (small animal ventilator, model 683; Harvard, South Natick, MA). End-expiratory CO 2 was continuously monitored by infrared CO 2 analyzer (model 2200; Heyer, Bad Ems, Germany). Mean arterial blood pressure (MABP) was measured by pressure transducer (Statham P23; Viggo-Spectramed, Oxnard, CA) connected to the femoral artery cannula. Arterial blood gases and hematocrit were determined before ic inoculation and every 2 h thereafter (gas check model 1304; Instrumentation Laboratory, Kirchheim, Germany). Body temperature was maintained at 38°C by a rectal thermometer-controlled heating pad. Rats were place...

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Factors influencing astrocyte growth and development in defined media

Cited by 94 publications

References 22 publications

Extracellular Heat Shock Protein 70: A Critical Component for Motoneuron Survival

Extracellular Heat Shock Protein 70: A Critical Component for Motoneuron Survival

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

Protective Effect of a 21-Aminosteroid during Experimental Pneumococcal Meningitis

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