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. 1997 Jun 1;17(11):4112-20.
doi: 10.1523/JNEUROSCI.17-11-04112.1997.

"V体育平台登录" Bone morphogenetic proteins induce astroglial differentiation of oligodendroglial-astroglial progenitor cells

P C Mabie  1 , M F Mehler, R Marmur, A Papavasiliou, Q Song, J A Kessler
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Bone morphogenetic proteins induce astroglial differentiation of oligodendroglial-astroglial progenitor cells

P C Mabie et al. J Neurosci. .

Abstract (V体育ios版)

We have used bipotent postnatal cortical oligodendroglial-astroglial progenitor cells (O-2As) to examine the role of inductive signals in astroglial lineage commitment. O-2A progenitor cells undergo progressive oligodendroglial differentiation when cultured in serum-free medium, but differentiate into astrocytes in medium supplemented with FBS. We now report that the bone morphogenetic proteins (BMPs), a major subclass of the transforming growth factor beta (TGFbeta) superfamily, promote the selective, dose-dependent differentiation of O-2As into astrocytes with concurrent suppression of oligodendroglial differentiation. This astroglial-inductive action is not sanctioned by other members of the TGFbeta superfamily. Astroglial differentiation requires only very brief initial exposure to the BMPs and is accompanied by increased cellular survival and accelerated exit from cell cycle. Dual-label immunofluorescence microscopy documents that O-2A progenitor cells express a complement of BMP type I and type II receptor subunits required for signal transduction. Furthermore, expression of BMP2 in vivo reaches maximal levels during the period of gliogenesis. These results suggest that the BMPs act as potent inductive factors in postnatal glial lineage commitment that initiate a stable program of astroglial differentiation. VSports手机版.

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Figures (V体育ios版)

Fig. 1.
Fig. 1.
Effect of BMP2 on O-2A differentiation. Photomicrographs of O-2As grown for 4 d with no added growth factor (A, C) or BMP2 (10 ng/ml) (B, D) and labeled with anti-GFAP (A, B) or GC/O1 (C,D). E, Photomicrograph of O-2A cells at the start of experimental manipulation labeled with anti-GD3. Scale bar, 65 μm.
Fig. 2.
Fig. 2.
Development of O-2A progenitors in the absence or presence of BMP2 (10 ng/ml). O-2As in SFM were analyzed for GFAP (A) or GC/O1 (B) immunoreactivity at days 1–4 and 7.
Fig. 3.
Fig. 3.
Effect of the BMPs on O-2A proliferation. O-2As treated with no added growth factor or BMP2 (10 ng/ml) were analyzed for BrdU incorporation by immunocytochemistry on 4 successive days.
Fig. 4.
Fig. 4.
O-2A dose responses to BMPs 2, 4, and 7. O-2As treated with no added growth factor or BMPs2, 4, or 7 at 0.1, 1, 10, or 30 ng/ml were grown for 4 d and analyzed for GFAP (A) and GC/O1 (B) immunoreactivity.
Fig. 5.
Fig. 5.
Comparison of BMP effects with other TGFβ cytokines. O-2As were treated with TGFβ1, activin, or GDNF (0.5 or 10 ng/ml) for 4 d, analyzed for GFAP and GC/O1 immunoreactivity, and compared with control and BMP2 (10 ng/ml)-treated cultures.
Fig. 6.
Fig. 6.
The effects of altered timing of BMP treatment on O-2A differentiation. A, Early withdrawal; cultures were treated with BMP2 (10 ng/ml) at the start of the experiment for 1, 24, 48, or 96 hr, washed three times, and replaced in SFM for the remainder of the experimental period. Controls remained untreated or treated with BMP2 (10 ng/ml) throughout the experimental period. After 7 d, cultures were analyzed for GFAP and GC/O1 immunoreactivity.B, Late addition; cultures were treated with BMP2 (10 ng/ml) after variable delays of 24, 48, or 96 hr and were analyzed as in A, using the same controls.
Fig. 7.
Fig. 7.
O-2A expression of BMP type I and type II receptor subunits. Photomicrographs of immunofluorescent dual-labeled O-2As with the lineage-specific antibody O4 (A,C, E) and antisera to BMPRII (B), BMPRIb (D), and BMPRIa (F). Each pair (A,B; C, D; E,F) represents the same field of view. Scale bar, 65 μm.
Fig. 8.
Fig. 8.
Expression of BMP2 in P8 and adult brain. Western blots were performed with a monoclonal antibody specific for BMP2. → Indicates the 116 kDa (unprocessed) form of BMP2.
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