S100B expression defines a state in which GFAP‐expressing cells lose their neural stem cell potential and acquire a more mature developmental stage

Abstract

During the postnatal development, astrocytic cells in the neocortex progressively lose their neural stem cell (NSC) potential, whereas this peculiar attribute is preserved in the adult subventricular zone (SVZ). To understand this fundamental difference, many reports suggest that adult subventricular GFAP-expressing cells might be maintained in immature developmental stage. Here, we show that S100B, a marker of glial cells, is absent from GFAP-expressing cells of the SVZ and that its onset of expression characterizes a terminal maturation stage of cortical astrocytic cells. Nevertheless, when cultured in vitro, SVZ astrocytic cells developed as S100B expressing cells, as do cortical astrocytic cells, suggesting that SVZ microenvironment represses S100B expression. Using transgenic s100b-EGFP cells, we then demonstrated that S100B expression coincides with the loss of neurosphere forming abilities of GFAP expressing cells. By doing grafting experiments with cells derived from beta-actin-GFP mice, we next found that S100B expression in astrocytic cells is repressed in the SVZ, but not in the striatal parenchyma. Furthermore, we showed that treatment with epidermal growth factor represses S100B expression in GFAP-expressing cells in vitro as well as in vivo. Altogether, our results indicate that the S100B expression defines a late developmental stage after which GFAP-expressing cells lose their NSC potential and suggest that S100B expression is repressed by adult SVZ microenvironment.

Aβ40 promotes neuronal cell fate in neural progenitor cells

“…After Ab40 or Ab42 treatment for 25 h, NPCs were fixed and stained for S100B, a marker for astrocyte development. 26 As shown in Figure 4, Ab42 significantly increased the number of S100B þ astrocytes compared to samples treated with Ab40 or the control sample treated with the vehicle DMSO.…”

Activity-dependent neuron–glial signaling by ATP and leukemia-inhibitory factor promotes hippocampal glial cell development

“…By 12 DIV, GFAP-expressing cells greatly increased, and accounted for 22 ± 1% of total cells (n = 34 cultures). This increase parallels astrocyte development in vivo (Catalani et al, 2002;Wei et al, 2002;Raponi et al, 2007).…”

Phenotypically aberrant astrocytes that promote motoneuron damage in a model of inherited amyotrophic lateral sclerosis

“…Cultured AbA cells are almost undistinguishable morphologically from primary neonatal astrocytes and exhibit a set of distinctive antigenic markers of undifferentiated astrocytes including high S100β and Cx43 expression and low levels of nonfilamentous GFAP. As a prototypic subunit of the calcium-binding S100 proteins, S100β is known to exert paracrine effects in astrocytes that contribute to proliferation, migration, differentiation, and neurotoxicity (28)(29)(30). Intracellular S100β can interact with GFAP monomers to prevent their assembly into filaments (31), possibly contributing to the diffuse GFAP distribution in AbA cells.…”