Serum modulates cyclic AMP-dependent morphological changes in cultured neurohypophysial astrocytes

Ramsell, Katrina D; Zhao, Bai Ge; Baker, Daniel L.; Cobbett, Peter

doi:10.1016/0361-9230(95)02057-8

Cited by 10 publications

(10 citation statements)

References 26 publications

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“…Calcium influx was blocked by equimolar replacement of Ca 2+ by Co 2+ in HBSS. As we have shown previously ( 8, 9) in pituicyte cultures incubated in HBSS supplemented only with forskolin, there was a significant increase in the fraction of stellate cells compared to cultures incubated in HBSS alone. Also, as shown previously ( 9), new born calf serum (0.5%) significantly reduced stellation induced by forskolin (forskolin‐induced stellation) and stellation occurring in cultures incubated in forskolin‐free HBSS (basal stellation; Fig.…”

Section: Resultssupporting

confidence: 82%

“…The plasticity of ultrastructural neuroglial relations in the neurohypophysis has been modelled using cultured pituicytes derived from adult rats. Cultured pituicytes may be induced to change from a protoplasmic, nonstellate form to a stellate form following activation of β‐adrenoreceptors ( 5–7) or by direct activation of adenylate cyclase by forskolin ( 8, 9). This stellation process was inhibited and rapidly reversed (destellation) when serum was included in the experimental medium in which the pituicyte cultures were incubated ( 9).…”

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confidence: 99%

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Calcium‐Independent, Tyrosine Phosphorylation‐Dependent Effects of Serum on the Morphology of Cultured Neurohypophysial Astrocytes

Ramsell

Cobbett

2000

J Neuroendocrinology

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Activation of adenylate cyclase induces cultured neurohypophysial astrocytes (pituicytes) to change from a protoplasmic, nonstellate form to a stellate form. Stellation is inhibited and reversed (destellation) by serum. The objective of the present studies was to examine the roles of Ca2+ and tyrosine phosphorylation in mediating these morphological changes. The effects of forskolin (to induce stellation) and serum (to inhibit and reverse stellation) were not affected by replacement of Ca2+ with Co2+ in the medium or by treatment of cultures with thapsigargin. However, genistein, a specific inhibitor of tyrosine kinase(s), significantly reduced the effect of serum on forskolin-induced stellation. Also, dephostatin, a specific inhibitor of tyrosine phosphatase, inhibited forskolin-induced stellation. In contrast, genistein did not have a dramatic effect on serum-induced destellation. The data demonstrate that morphological changes exhibited by cultured pituicytes are independent of Ca2+ but may be modulated by the activity of tyrosine kinase(s) and phosphatase(s).

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Section: Resultssupporting

confidence: 82%

mentioning

confidence: 99%

Calcium‐Independent, Tyrosine Phosphorylation‐Dependent Effects of Serum on the Morphology of Cultured Neurohypophysial Astrocytes

Ramsell

Cobbett

2000

J Neuroendocrinology

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“…1A). Serum and serum components induce a polygonal morphology in astrocytes, and, when the serum concentration in the media is reduced, the cells are converted to a stellate shape (Ramsell et al, 1996). Previous studies have demonstrated that treatment with propentofylline induces stellation (Tawfik et al, 2006), indicative of the drug driving the astrocytes to a less active state.…”

Section: Resultsmentioning

confidence: 99%

“…Astrocytes show a reactive morphology and proliferate when maintained in cell culture media containing fetal bovine serum (FBS; Ramsell et al, 1996), and rapamycin, an mTORC1 inhibitor, prevents FBS‐induced astrocyte proliferation (Codeluppi et al, 2009). Furthermore, it was recently shown that TNF enhances proliferation of astrocytes cultured in low‐serum media (Cui et al, 2011) and that TNF induces signaling through the MAPK and NFκB pathways.…”

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confidence: 99%

Pentoxifylline and propentofylline prevent proliferation and activation of the mammalian target of rapamycin and mitogen activated protein kinase in cultured spinal astrocytes

Gregory

Delaney

Abdelmoaty

et al. 2012

J of Neuroscience Research

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Astrocyte activation is an important feature in many disorders of the central nervous system, including chronic pain conditions. Activation of astrocytes is characterized by a change in morphology, including hypertrophy and increased size of processes, proliferation, and an increased production of proinflammatory mediators. The xanthine derivatives pentoxifylline and propentofylline are commonly used experimentally as glial inhibitors. These compounds are generally believed to attenuate glial activity by raising cyclic AMP (cAMP) levels and inhibiting glial tumor necrosis factor (TNF) production. In the present study, we show that these substances inhibit TNF and serum-induced astrocyte proliferation and signaling through the mammalian target of rapamycin (mTOR) pathway, demonstrated by decreased levels of phosphorylated S6 kinase (S6K), commonly used as a marker of mTOR complex (mTORC) activation. Furthermore, we show that pentoxifylline and propentofylline also inhibit JNK and p38, but not ERK, activation induced by TNF. In addition, the JNK antagonist SP600125, but not the p38 inhibitor SB203580, prevents TNF-induced activation of S6 kinase, suggesting that pentoxifylline and propentofylline may regulate mTORC activity in spinal astrocytes partially through inhibition of the JNK pathway. Our results suggest that pentoxifylline and propentofylline inhibit astrocyte activity in a broad fashion by attenuating flux through specific pathways.

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“…Pituicyte cultures were prepared as previously described [31]. Eight weeks old Wistar adult male rats were deeply anesthetized by CO 2 inhalation and decapitated in accordance with French/European ethical guidelines.…”

Section: Pituicytes Cell Culturementioning

confidence: 99%

Expression of Dystrophins and the Dystrophin-Associated-Protein Complex by Pituicytes in Culture

et al. 2011

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The dystrophin-associated-protein complex (DAPC) has been extensively characterized in the central nervous system where it is localized both in neuronal and glial cells. Few studies have characterized this complex in the neurohypophysis. To further study this complex in pituicytes, the resident astroglia of the neurophypophysis, we used adult pituicyte cultures and determined the expression and localization of dystrophins/utrophins and the DAPC by RT-PCR, western blotting and immunofluorescence. Our data show that the pituicytes express dystrophins, utrophins and several members of the DAPC including dystroglycans, δ-, γ-sarcoglycans, α-dystrobrevin-1 and α1-syntrophin. Double immunofluorescence analysis shows that laminin colocalizes with dystroglycan, suggesting that similarly to muscle and astrocytes, the DAPC interacts with the extracellular matrix in pituicytes. Collectively these findings show that dystrophins/utrophins and members of the DAPC are expressed in pituicytes where they may form multiprotein complexes and play a role in the retraction-reinsertion of pituicyte endfeet during specific physiological conditions.

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Serum modulates cyclic AMP-dependent morphological changes in cultured neurohypophysial astrocytes

Cited by 10 publications

References 26 publications

Calcium‐Independent, Tyrosine Phosphorylation‐Dependent Effects of Serum on the Morphology of Cultured Neurohypophysial Astrocytes

Calcium‐Independent, Tyrosine Phosphorylation‐Dependent Effects of Serum on the Morphology of Cultured Neurohypophysial Astrocytes

Pentoxifylline and propentofylline prevent proliferation and activation of the mammalian target of rapamycin and mitogen activated protein kinase in cultured spinal astrocytes

Expression of Dystrophins and the Dystrophin-Associated-Protein Complex by Pituicytes in Culture

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