Tenascin-C regulates proliferation and migration of cultured astrocytes in a scratch wound assay

Nishio, Takeshi; Kawaguchi, Saburo; Yamamoto, Masaki; Iseda, Tsutomu; Kawasaki, Takayuki; Hase, Takao

doi:10.1016/j.neuroscience.2004.12.028

Cited by 79 publications

(63 citation statements)

References 48 publications

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“…1). Although expression of TnC bordering areas of dynamic cell movements and interactions has been well documented during development (Steindler et al, 1995) and after injury (Laywell et al, 1992;Gates et al, 1996;Nishio et al, 2005), its role remains elusive (Nishio et al, 2005). The only difference we detected within the SEZ of the TnC deficient mice was the increased number of type-A cell clusters along the LV wall.…”

Section: Discussionmentioning

confidence: 74%

“…Tenascin-C (TnC) is a large ECM glycoprotein (Jones and Jones, 2000) that is expressed in the brain neurogenic zones during development (Steindler et al, 1995;Garcion et al, 2004) and postnatally (Thomas et al, 1996;Garcion et al, 2001;Peretto et al, 2005;Bonnert et al, 2006;de Chevigny et al, 2006) as well as in areas of plasticity (i.e., after injury) in the adult brain (Laywell et al, 1992;Gates et al, 1996;Nishio et al, 2005). This expression profile combined with results using TnC null mice showing a role for TnC in the proliferation and migration of early postnatal neural precursors (Garcion et al, 2001) and the growth-factor responsiveness of embryonic neural stem cells (NSC) (Garcion et al, 2004) led us to ask whether TnC also plays a role in adult neurogenesis.…”

Section: Introductionmentioning

confidence: 99%

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The Adult Mouse Subependymal Zone Regenerates Efficiently in the Absence of Tenascin-C

Kazanis¹,

Belhadi²,

Faissner³

et al. 2007

J. Neurosci.

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The subependymal zone (SEZ) of the lateral ventricles of the adult mouse brain hosts neurogenesis from a neural stem cell population with the morphology of astrocytes (termed type-B cells). Tenascin-C is a large extracellular matrix glycoprotein present in the SEZ that has been shown to regulate the development of embryonic neural stem cells and the proliferation and migration of early postnatal neural precursors. Here we show that tenascin-C is produced by type-B cells and forms a layer between SEZ and the adjacent striatum. Tenascin-C deficiency resulted in minor structural differences in and around the SEZ. However, the numbers of neural stem cells and their progeny remained unaffected, as did their regeneration after depletion of mitotic cells using the antimitotic drug cytosine-␤-Darabinofuranoside. Our results reveal a remarkable ability of the adult neural stem cell niche to retain proper function even after the removal of major extracellular matrix molecules.

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Section: Discussionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 99%

The Adult Mouse Subependymal Zone Regenerates Efficiently in the Absence of Tenascin-C

Kazanis¹,

Belhadi²,

Faissner³

et al. 2007

J. Neurosci.

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“…Although the role of integrin-ECM adhesions in mechanotransduction have been well-characterized in other cell types (Katsumi et al, 2004), a link between integrin-mediated astrogliotic alterations and biomechanical inputs has not been established. However, integrins have been shown to play a significant role in astrocyte migration and proliferation (Etienne-Manneville and Hall, 2001;Nishio et al, 2005), suggesting that mechanical stimulation of these receptors may contribute to the astrogliotic response to mechanical injury. Although our results demonstrate a strain rate-dependence in astrogliotic responses, the role of mechanotransduction as it relates to TBI has not been well-studied and will require further investigation.…”

Section: Discussionmentioning

confidence: 99%

Strain rate-dependent induction of reactive astrogliosis and cell death in three-dimensional neuronal–astrocytic co-cultures

2007

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A mechanical insult to the brain drastically alters the microenvironment as specific cell types become reactive in an effort to sequester severely damaged tissue. Although injury-induced astrogliosis has been investigated, the relationship between well-defined biomechanical inputs and acute astrogliotic alterations are not well understood. We evaluated the effects of strain rate on cell death and astrogliosis using a three-dimensional (3-D) in vitro model of neurons and astrocytes within a bioactive matrix. At 21 days post-plating, co-cultures were deformed to 0.50 shear strain at strain rates of 1, 10, or 30 s −1 . We found that cell death and astrogliotic profiles varied differentially based on strain rate at two days post-insult. Significant cell death was observed after moderate (10 s −1 ) and high (30 s −1 ) rate deformation, but not after quasi-static (1 s −1 ) loading. The vast majority of cell death occurred in neurons, suggesting these cells are more susceptible to high rate shear strains than astrocytes for the insult parameters used here. Injury-induced astrogliosis was compared to co-cultures treated with transforming growth factor β, which induced robust astrocyte hypertrophy and increased glial fibrillary acidic protein (GFAP) and chondroitinsulfate proteoglycans (CSPGs). Quasi-static loading resulted in increased cell density and CSPG secretion. Moderate rate deformation increased cell density, GFAP reactivity, and hypertrophic process density. High rate deformation resulted in increased GFAP reactivity; however, other astrogliotic alterations were not observed at this time-point. These results demonstrate that the mode and degree of astrogliosis depend on rate of deformation, demonstrating astrogliotic augmentation at sub-lethal injury levels as well as levels inducing cell death.

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“…Analysis of cell migratory behavior in vitro in response to chemical agents, genetic manipulations, or molecule-coated surfaces is used to dissect mechanisms that occur during development, normal physiological responses, or abnormal pathological conditions (Gavert et al 2005;Petridis et al 2004;Nishio et al 2005;Yoshida et al 2004;Zhang et al 2005;Herren et al 2001;Lee et al 2004;Maschler et al 2005;Zhu et al 2004;Moyano et al 2003). Many analyses, however, lack ability to analyze individual cells, precision of measurements, or temporal resolution.…”

Section: Introductionmentioning

confidence: 99%

Automated time-lapse microscopy and high-resolution tracking of cell migration

et al. 2006

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We describe a novel fully automated high-throughput time-lapse microscopy system and evaluate its performance for precisely tracking the motility of several glioma and osteoblastic cell lines. Use of this system revealed cell motility behavior not discernable with conventional techniques by collecting data (1) from closely spaced time points (minutes), (2) over long periods (hours to days), (3) from multiple areas of interest, (4) in parallel under several different experimental conditions. Quantitation of true individual and average cell velocity and path length was obtained with high spatial and temporal resolution in ''scratch'' or ''wound healing'' assays. This revealed unique motility dynamics of drug-treated and adhesion molecule-transfected cells and, thus, this is a considerable improvement over current methods of measurement and analysis. Several fluorescent vital labeling methods commonly used for end-point analyses (GFP expression, DiO lipophilic dye, and Qtracker nanocrystals) were found to be useful for timelapse studies under specific conditions that are described. To illustrate one application, fluorescently labeled tumor cells were seeded onto cell monolayers expressing ectopic adhesion molecules, and this resulted in consistently reduced tumor cell migration velocities. These highly quantitative time-lapse analysis methods will promote the creation of new cell motility assays and increase the resolution and accuracy of existing assays.

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Tenascin-C regulates proliferation and migration of cultured astrocytes in a scratch wound assay

Cited by 79 publications

References 48 publications

The Adult Mouse Subependymal Zone Regenerates Efficiently in the Absence of Tenascin-C

The Adult Mouse Subependymal Zone Regenerates Efficiently in the Absence of Tenascin-C

Strain rate-dependent induction of reactive astrogliosis and cell death in three-dimensional neuronal–astrocytic co-cultures

Automated time-lapse microscopy and high-resolution tracking of cell migration

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