Re-expression of the intermediate filament nestin in reactive astrocytes

In vitro growth and differentiation of canine olfactory bulb-derived neural progenitor cells under variable culture conditions

“…However, astrocytes derived from neurospheres maintained in EGF, were positive for GFAP, nestin, Map2 and Tau (Schinstine and Iacovitti, 1996). In mice, cortical injury studies suggest that nestin + cells migrate from the subventricular zone to the site of injury (Frisen et al, 1995;Lin et al, 1995). Thus, the Map2ab + cells with immature morphology in the OB-cNPC cultures may represent a cell type analogous to reactive astrocytes.…”

“…It has previously been shown that subsequent to CNS injury, reactive astrocytes can express the neuronal antigens Tau, Map2, neuron-specific enolase, and GABA, in addition to GFAP and nestin (Lin and Matesic, 1994;Frisen et al, 1995;Schinstine and Iacovitti, 1996;Sahin Kaya et al, 1999). It has been hypothesized that reactive astrocytes represent either astrocytes that revert to bipotential progenitors (cells that show both neuronal and glial phenotypes) or that reactive astrocytes are recruited from neural stem cells (Lin et al, 1995;Schinstine and Iacovitti, 1996). Evidence to support the latter comes from both in vitro and in vivo studies.…”

Transforming growth factor α promotes sequential conversion of mature astrocytes into neural progenitors and stem cells

“…Upon nerve injury, these glial cells of the peripheral nervous system de-differentiate into their immediate precursors before proliferating and differentiating into myelinating mature cells (Scherer, 1997). Although the upregulation of the intermediate filament nestin and its isoform RC2, normally present in progenitors, and enhanced TGFa synthesis, have been reported in astrocytes following CNS injury (Frisen et al, 1995;Lin et al, 1995;Leavitt et al, 1999;Junier, 2000), their capability to behave in situ as regenerative cells remains to be uncovered. However, contrary to Schwann cells, astrocytes do not respond to injury by entering en masse into the cell cycle, and this tight control of their proliferation (Norenberg, 1994;Dihne et al, 2001) might limit their in vivo plasticity.…”

Glycan-dependent binding of galectin-1 to neuropilin-1 promotes axonal regeneration after spinal cord injury

“…However, Gal-1 treatment induced profound changes in the phenotype of GFAP-positive cells. Reexpression of nestin intermediate filaments was observed in reactive astrocytes, 28 which were selectively distributed in areas surrounding the lesion but not in the lesion itself. Gal-1 treatment induced sharp alterations in the morphology of nestin-positive cells, revealing a strong reduction in cellular processes.…”