Pituicyte Stellation is Prevented by RhoA-or Cdc42-Dependent Actin Polymerization

Rosso, Lia; Pierson, Patricia; Golfier, Claire; Peteri-Brünback, Brigitta; Deroanne, Christophe; Obberghen-Schilling, Ellen Van; Mienville, Jean-Marc

doi:10.1007/s10571-007-9176-7

Cited by 14 publications

(11 citation statements)

References 25 publications

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“…Rho A also plays an important role in the regulation of cytoskeletal organization [20]. Recently, there has been increasing evidence supporting that the inactivation of Rho A and its downstream effectors effectively induced astrocytes stellation [32,[38][39][40]. Consistent with these findings, we found the expression of Rho A decreased and that LPA, an activator of Rho A [11], partly suppressed lactacystininduced stellation.…”

Section: Discussionsupporting

confidence: 87%

Lactacystin Stimulates Stellation of Cultured Rat Cortical Astrocytes

Ren

Pan

et al. 2008

Neurochem Res

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Proteasome inhibition has been observed in many neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Here, the effect of proteasome inhibition on the morphology of cultured rat cortical astrocytes was investigated. Increasing evidence suggests that the function of astrocytes is related closely to its morphology. Lactacystin, a specific inhibitor of the 20S proteasome, can induce astrocytes stellation in a dose dependent manner and reorganize the cytoskeleton of astrocytes. Furthermore, decreased levels of expression of Rho A, total Akt, and Phospho-Akt were found in the process of astrocytes stellation and lysophosphatidic acid, an activator of Rho A, can largely reverse the astrocytes stellation caused by lactacystin. This suggests that proteasome inhibition in astrocytes could stabilize signals of morphological changes that might be processed through Rho and Akt signaling cascade. Our results suggest that proteasome inhibition might function as a factor regulating astrocytes morphology in some pathophysiological conditions.

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Section: Discussionsupporting

confidence: 87%

Lactacystin Stimulates Stellation of Cultured Rat Cortical Astrocytes

Ren

Pan

et al. 2008

Neurochem Res

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“…Whether the balance of small GTPases governs also stellation, however, was still an open question. RhoA activation had been shown to induce reconversion of stellate to flat cells (Suidan et al, 1997), and inhibition of RhoA and/or of ROCK to be needed for stellation to occur (Boran and Garcia, 2007; Favero and Mandel, 2007; Hotje et al, 2005; John et al, 2004; Rosso et al, 2007). Yet, results obtained by various approaches had suggested Rac1 not to be involved (John et al, 2004; Lichtenstein etal., 2010; Rosso et al, 2007; Suidan et al, 1997; see however Salhia et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Soon thereafter, cultured astrocytes were found to reacquire at least part of their in situ phenotype, with reduction of the cell body and outgrowth of processes, when exposed to either dibutyryl cAMP (db-cAMP) or brain extracts in serum-free medium (Lin et al, 1973; Lin and Mitsunobu, 1974; Moonen et al, 1975). The process, often named stellation, was shown to be induced also by other agents: cGMP, administered as the 8-bromo analogue (8Br-cGMP) or generated in response to the atrial natriuretic peptide (Boran and Garcia, 2007); AICAR, an activator of the AMP-dependent protein kinase (Favero and Mandel, 2007); interleukin 1β (John et al, 2004); ATP (Neary et al, 1994) acting via activation of the adenosine A2 receptor (Rosso et al, 2007); various nonsteroidal anti-inflammatory agents (Lichtenstein et al, 2010); botulinum toxin C3 (Suidan et al, 1997). Conversely, flattening of stellate astrocytes was induced not only by serum but also by thrombin and lysophosphatidic acid (Holtje et al, 2005; Suidan et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

“…High Rho and ROCK activities are necessary for flattening; repression of RhoA (Boran and Garcia, 2007; Holtje et al, 2005; John et al, 2005; Rosso et al, 2007) or blockade of ROCK (Abe and Misawa, 2003; John et al, 2005; Lau et al, 2011; Salhia et al, 2005) induce the conversion of flat to stellate astrocytes. The expansion or marked reduction of the cell body accompanied by the disappearance or outgrowth of branched processes, respectively, are sustained by the reshaping of the cytoskeleton, a well-known target of Rho GTPases (Hall, 2005; Ridley, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…Rac 1 is known to govern dendritic outgrowth in various types of neural cells (Hirose et al, 1998; Racchetti et al, 2010). In astrocytes, studies had been carried out, however with conflicting results (John et al, 2005; Lichtenstein et al 2010; Rosso et al, 2007; Salhia et al, 2005; Suidan et al, 1997). The second issue concerns the nature and trafficking of the membranes necessary for stellation and flattening to occur.…”

Section: Introductionmentioning

confidence: 99%

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Astrocyte stellation, a process dependent on Rac1 is sustained by the regulated exocytosis of enlargeosomes

Racchetti¹,

D’Alessandro

Meldolesi³

2011

Glia

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Cultured astrocytes exhibit a flat/epitelioid phenotype much different from the star-like phenotype of tissue astrocytes. Upon exposure to treatments that affect the small GTPase Rho and/or its effector ROCK, however, flat astrocytes undergo stellation, with restructuring of cytoskeleton and outgrowth of processes with lamellipodia, assuming a phenotype closer to that exhibited in situ. The mechanisms of this change are known only in part. Using the ROCK blocker drug Y27632, which induces rapid (tens of min), dose-dependent and reversible stellations, we focused on two specific aspects of the process: its dependence on small GTPases and the large surface expansion of the cells. Contrary to previous reports, we found stellation to be governed by the small G protein Rac1, up to disappearance of the process when Rac1 was downregulated or blocked by a specific drug. In contrast cdc42, the other G-protein often involved in phenotype changes, appeared not involved. The surface expansion concomitant to cytoskeleton restructuring, also dependent on Rac1, was found to be at least partially sustained by the exocytosis of enlargeosomes, small vesicles distinct from classical cell organelles, which are abundant in astrocytes. Exhaustion of stellation induced by repeated administrations of Y27632 correlated with the decrease of the enlargeosome pool. A whole-cell process like stellation of cultured astrocytes might be irrelevant in the brain tissue. However, local restructuring of the cytoskeleton coordinate with surface expansion, occurring at critical cell sites and sustained by mechanisms analogous to those of stellation, might be of importance in both astrocyte physiology and pathology. © 2011 Wiley Periodicals, Inc.

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Pituicyte modulation of neurohormone output

Rosso

Mienville

2008

Glia

Self Cite

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Pituicytes have long been suspected to play a role in the regulation of neurohypophysial hormone output. This role has been mainly ascribed to morphological changes in these cells and subsequent modifications of their tight structural relationships with surrounding nerve terminals and capillaries. These entirely reversible changes are brought about by physiological states such as parturition, lactation, or dehydration, and it was inferred that they should facilitate neurohormone output, based on concerted analyses of in vitro, in situ, and ex vivo experiments. Pituicyte stellation, the in vitro counterpart of these morphological changes, can be induced by beta-adrenergic or A1-adenosine receptor activation, and appears to result from inhibition of the small GTPase RhoA. Actin depolymerization is the key event allowing stellation. Vasopressin and oxytocin reverse stellation and return pituicytes to their basal shape by activating Cdc42, another small GTPase that reorganizes the actin cytoskeleton in a cortical position. Adenosine and neurohormones also have opposite actions on the efflux of taurine, a local messenger that is released by pituicytes in hypotonic conditions and accordingly inhibits vasopressin output from axon terminals. As adenosine is likely generated from endogenous ATP co-released with neurohormones and broken down by local ectoATPases, these data suggest a subtle balance between a positive and a negative feedback on vasopressin output operated, respectively, by adenosine and vasopressin to maintain hydromineral homeostasis. A theoretical scenario is presented to account for the putative sequence of pituicyte-related events following disturbance of the hydromineral system.

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Pituicyte Stellation is Prevented by RhoA-or Cdc42-Dependent Actin Polymerization

Cited by 14 publications

References 25 publications

Lactacystin Stimulates Stellation of Cultured Rat Cortical Astrocytes

Lactacystin Stimulates Stellation of Cultured Rat Cortical Astrocytes

Astrocyte stellation, a process dependent on Rac1 is sustained by the regulated exocytosis of enlargeosomes

Pituicyte modulation of neurohormone output

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