Vimentin-expressing proximal reactive astrocytes correlate with migration rather than proliferation following focal brain injury

Wang, Kai; Bekar, Lane K.; Furber, Kendra L.; Walz, Wolfgang

doi:10.1016/j.brainres.2004.07.086

Cited by 47 publications

(40 citation statements)

References 44 publications

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“…Hsp-70 expression in natural killer cells increases their migration [Gastpar et al, 2004]. Expression of vimentin, a cytosolic protein, is known to increase cell motility [Wang et al, 2004]. These data suggest that ubiquitous calpains regulate Hsp-70 and vimentin expression levels.…”

Section: Discussionmentioning

confidence: 96%

Myoblast attachment and spreading are regulated by different patterns by ubiquitous calpains

Mazères¹,

Leloup²,

Daury³

et al. 2006

Cell Motil. Cytoskeleton

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The calcium-dependent proteolytic system is a large family of well-conserved ubiquitous and tissue-specific proteases, known as calpains, and an endogenous inhibitor, calpastatin. Ubiquitous calpains are involved in many physiological phenomena, such as the cell cycle, muscle cell differentiation, and cell migration. This study investigates the regulation of crucial steps of cell motility, myoblast adhesion and spreading, by calpains. Inhibition of each ubiquitous calpain isoform by antisense strategy pinpointed the involvement of each of these proteases in myoblast adhesion and spreading. Moreover, the actin cytoskeleton and microtubules were observed in transfected cells, demonstrating that each ubiquitous calpain could be involved in the actin fiber organization. C2C12 cells with reduced mu- or m-calpain levels have a rounded morphology and disorganized stress fibers, but no modification in the microtubule cytoskeleton. Antisense strategy directed against MARCKS, a calpain substrate during C2C12 migration, showed that this protein could play a role in stress fiber polymerization. A complementary proteomic analysis using C2C12 cells over-expressing calpastatin indicated that two proteins were under-expressed, while six, which are involved in the studied phenomena, were overexpressed after calpain inhibition. The possible role of these proteins in adhesion, spreading, and migration was discussed.

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Section: Discussionmentioning

confidence: 96%

Myoblast attachment and spreading are regulated by different patterns by ubiquitous calpains

Mazères¹,

Leloup²,

Daury³

et al. 2006

Cell Motil. Cytoskeleton

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show abstract

“…Alonso (2001) demonstrated a positive correlation between Vim expression and neural progenitor proliferation in both the subgranular zone and subventricular zone. However, no direct link is known between Vim expression and the proliferation/ differentiation of astrocytes in other regions (Khurgel et al, 1995;Stringer, 1996;Wang and Walz, 2003;Wang et al, 2004;Revuelta et al, 2005). In addition, Vim reexpressed mature astrocytes have a radial glia-like function and guide migratory cells (Wang and Walz, 2003;Wang et al, 2004 (Niquet et al, 1994a,b;Wang et al, 2004;Kang et al, 2006;Parent et al, 2006).…”

Section: Astroglial Proliferation/gliogenesis In Epilepsymentioning

confidence: 96%

“…However, no direct link is known between Vim expression and the proliferation/ differentiation of astrocytes in other regions (Khurgel et al, 1995;Stringer, 1996;Wang and Walz, 2003;Wang et al, 2004;Revuelta et al, 2005). In addition, Vim reexpressed mature astrocytes have a radial glia-like function and guide migratory cells (Wang and Walz, 2003;Wang et al, 2004 (Niquet et al, 1994a,b;Wang et al, 2004;Kang et al, 2006;Parent et al, 2006). Therefore, the present data suggest that reactive astrogliosis in different parts of the hippocampo- The quantitative analyses of excitability ratio (ER ϭ PS1/EPSP1, left panels) and population spike amplitude ratio (PSR ϭ PS2/PS1, right panels) in the dentate gyrus (C,D) and the CA1 (E,F) after AA infusion (mean Ϯ SEM).…”

Section: Astroglial Proliferation/gliogenesis In Epilepsymentioning

confidence: 98%

Spatiotemporal characteristics of astroglial death in the rat hippocampo‐entorhinal complex following pilocarpine‐induced status epilepticus

Kim

Kwak

et al. 2008

J of Comparative Neurology

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Recently we reported that astroglial loss and subsequent gliogenesis in the dentate gyrus play a role in epileptogenesis following pilocarpine-induced status epilepticus (SE). In the present study we investigated whether astroglial damages in the hippocampo-entorhinal complex following SE are relevant to pathological or electrophysiological properties of temporal lobe epilepsy. Astroglial loss/damage was observed in the entorhinal cortex and the CA1 region at 4 weeks and 8 weeks after SE, respectively. These astroglial responses in the hippocampo-entorhinal cortex were accompanied by hyperexcitability of the CA1 region (impairment of paired-pulse inhibition and increase in excitability ratio). Unlike the dentate gyrus and the entorhinal cortex, CA1 astroglial damage was protected by conventional anti-epileptic drugs. alpha-Aminoadipic acid (a specific astroglial toxin) infusion into the entorhinal cortex induced astroglial damage and changed the electrophysiological properties in the CA1 region. Astroglial regeneration in the dentate gyrus and the stratum oriens of the CA1 region was found to originate from gliogenesis, while that in the entorhinal cortex and stratum radiatum of the CA1 region originated from in situ proliferation. These findings suggest that regional specific astroglial death/regeneration patterns may play an important role in the pathogenesis of temporal lobe epilepsy.

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“…To determine whether the AQP4-dependent astroglial cell migration in culture models might occur in the brain in vivo, we studied reactive gliosis and glial scar formation using a well-established cortical-stab-injury model (Bush et al, 1999;Hampton et al, 2004;Rhodes et al, 2003;Wang et al, 2004). The stab-injury mouse model, unlike other brain-injury models (tumor, infection, trauma), is not associated with significant brain swelling, which could confound interpretation of results.…”

Section: Reactive Gliosis In Vivomentioning

confidence: 99%

Involvement of aquaporin-4 in astroglial cell migration and glial scar formation

Saadoun

Papadopoulos

Watanabe

et al. 2005

Journal of Cell Science

430

386

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Aquaporin-4, the major water-selective channel in astroglia throughout the central nervous system, facilitates water movement into and out of the brain. Here, we identify a novel role for aquaporin-4 in astroglial cell migration, as occurs during glial scar formation. Astroglia cultured from the neocortex of aquaporin-4-null mice had similar morphology, proliferation and adhesion, but markedly impaired migration determined by Transwell migration efficiency (18±2 vs 58±4% of cells migrated towards 10% serum in 8 hours; P<0.001) and wound healing rate (4.6 vs 7.0 μm/hour speed of wound edge; P<0.001) compared with wild-type mice. Transwell migration was similarly impaired (25±4% migrated cells) in wild-type astroglia after ∼90% reduction in aquaporin-4 protein expression by RNA inhibition. Aquaporin-4 was polarized to the leading edge of the plasma membrane in migrating wild-type astroglia, where rapid shape changes were seen by video microscopy. Astroglial cell migration was enhanced by a small extracellular osmotic gradient, suggesting that aquaporin-4 facilitates water influx across the leading edge of a migrating cell. In an in vivo model of reactive gliosis and astroglial cell migration produced by cortical stab injury, glial scar formation was remarkably impaired in aquaporin-4-null mice, with reduced migration of reactive astroglia towards the site of injury. Our findings provide evidence for the involvement of aquaporin-4 in astroglial cell migration, which occurs during glial scar formation in brain injury, stroke, tumor and focal abscess.

show abstract

Vimentin-expressing proximal reactive astrocytes correlate with migration rather than proliferation following focal brain injury

Cited by 47 publications

References 44 publications

Myoblast attachment and spreading are regulated by different patterns by ubiquitous calpains

Myoblast attachment and spreading are regulated by different patterns by ubiquitous calpains

Spatiotemporal characteristics of astroglial death in the rat hippocampo‐entorhinal complex following pilocarpine‐induced status epilepticus

Involvement of aquaporin-4 in astroglial cell migration and glial scar formation

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