Neuronal Progenitor Cells Derived from the Anterior Subventricular Zone of the Neonatal Rat Forebrain Continue to Proliferatein Vitroand Express a Neuronal Phenotype

Luskin, Marla B.; Zigova, Tanja; Soteres, B. J.; Stewart, Randall R.

doi:10.1006/mcne.1996.0592

Cited by 177 publications

(131 citation statements)

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“…The localization of ␤III in immature neuroepithelial cells, including precursor cells of the SVZ, is presently construed as a priori evidence of neuronal lineage differentiation [Lee et al, 1990b;Fanarraga et al, 1999;Menezes and Luskin, 1994;Gates et al, 1995;Luskin et al, 1997;Peretto et al, 1997;Doetsch et al, 1997;Hatanaka and Jones, 1998;Grever et al, 1999;Brannen andSugaya, 2000, Brazelton et al, 2000;Gould et al, 2001]. It has been asserted that subpopulations of immature neuroepithelial cells co-expressing the polysialated form (PSA)-NCAM and ␤III in the anterior SVZ of human infants are presumptive neurons [Weickert et al, 2000].…”

Section: Class III ␤-Tubulin In the Context Of Telencephalic (Forebramentioning

confidence: 99%

Class III β‐tubulin in human development and cancer

Katsetos

Herman²,

Mörk

2003

Cell Motil. Cytoskeleton

254

188

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The differential cellular expression of class III ␤-tubulin isotype (␤III) is reviewed in the context of human embryological development and neoplasia. As compared to somatic organs and tissues, ␤III is abundant in the central and peripheral nervous systems (CNS and PNS) where it is prominently expressed during fetal and postnatal development. As exemplified in cerebellar and sympathoadrenal neurogenesis, the distribution of ␤III is neuron-associated, exhibiting distinct temporospatial gradients according to the regional neuroepithelia of origin. However, transient expression of this protein is also present in the subventricular zones of the CNS comprising putative neuronal-and/or glial precursor cells, as well as in Kulchitsky neuroendocrine cells of the fetal respiratory epithelium. This temporally restricted, potentially non-neuronal expression may have implications in the identification of presumptive neurons derived from embryonic stem cells. In adult tissues, the distribution of ␤III is almost exclusively neuron-specific. Altered patterns of expression are noted in cancer. In "embryonal"-and "adult-type" neuronal tumors of the CNS and PNS, ␤III is associated with neuronal differen- Abbreviations: bHLH, basic helix-loop-helix; ␤III, class III ␤-tubulin isotype, CNE , central nervous system enhancer; CNS, central nervous system; EGL, external granule layer; MAP, microtubule-associated protein; NCAM, neural cell adhesion molecule; OPC, oligodendrocyte precursor cell; PCNA, proliferating cell nuclear antigen; PNS, peripheral nervous system; pRb, retinoblastoma tumor suppressor protein; PSA, polysialated; SVZ, subventricular zone; WHO, World Health Organization. tiation and decreased cell proliferation. In contrast, the presence of ␤III in gliomas and lung cancer is associated with an ascending histological grade of malignancy. Thus, ␤III expression in neuronal tumors is differentiation-dependent, while in non-neuronal tumors it is aberrant and/or represents "dedifferentiation" associated with the acquisition of progenitor-like phenotypic properties. Increased expression in various epithelial cancer cell lines is associated with chemoresistance to taxanes. Because ␤III is present in subpopulations of neoplastic, but not in normal differentiated glial or somatic epithelial cells, the elucidation of mechanisms responsible for the altered expression of this isotype may provide insights into the role of the microtubule cytoskeleton in tumorigenesis and tumor progression. Cell Motil. Cytoskeleton 55: 77-96, 2003.

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Section: Class III ␤-Tubulin In the Context Of Telencephalic (Forebramentioning

confidence: 99%

Class III β‐tubulin in human development and cancer

Katsetos

Herman²,

Mörk

2003

Cell Motil. Cytoskeleton

254

188

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“…Unlike the well-studied progenitor cells of the embryonic telencephalic ventricular zone (VZ), which give rise to the neurons of the cerebral cortex (McConnell, 1989;Luskin, 1994), SVZa-derived cells initiate differentiation without becoming postmitotic (Menezes et al, 1995;Luskin et al, 1997;Coskun et al, 2001b). This property of the SVZa cells prompted us to examine whether they regulate their cell cycle in a fashion different from that of other CNS progenitor cells.…”

Section: Svza Neuronal Progenitor Cells Successively Undergo Rounds Omentioning

confidence: 99%

“…The unique progenitor cells, referred to as SVZa cells, are located in a restricted portion of the SVZ surrounding the anterior part of the lateral ventricles of the forebrain ( Fig. 1A; Luskin, 1993;Luskin et al, 1997). The SVZa is contiguous with a band of cells, the rostral migratory stream (RMS), which extends into the middle of the olfactory bulb.…”

mentioning

confidence: 99%

Intrinsic and extrinsic regulation of the proliferation and differentiation of cells in the rodent rostral migratory stream

Coskun

Luskin

2002

J of Neuroscience Research

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An overriding principle of development is that neurons become permanently postmitotic once they initiate differentiation. Work in our laboratory, however, has provided evidence for a population of progenitor cells in mammalian forebrain that express properties of differentiated neurons, even though they continue to divide. These neuronal progenitor cells are situated in the rostral migratory stream (RMS), which extends from a specialized portion of the subventricular zone surrounding the anterior tip of the lateral ventricle, referred to as the SVZa, to the middle of the olfactory bulb. As SVZa‐derived cells migrate to the olfactory bulb, they undergo cell division, and they never deviate from the RMS. Once they reach their final destinations, they become terminally postmitotic interneurons. This Mini‐Review concerns findings from our recent experiments designed to reveal the intrinsic and extrinsic mechanisms governing the proliferation and differentiation of the unique SVZa neuronal progenitor cells. We have investigated the role(s) of cell cycle regulatory proteins, in particular, the cell cycle inhibitor p19INK4d, in the control of SVZa cell proliferation. Several studies have indicated that cells withdraw from the cell cycle once they express p19INK4d. To begin to investigate whether p19INK4d(+) SVZa‐derived cells are postmitotic, we analyzed the pattern of p19INK4d expression by the cells of the RMS. A pronounced gradient of p19INK4d expression was demonstrated; progressively more cells are p19INK4d immunoreactive as the olfactory bulb is approached. In addition, the capacity of p19INK4d(+) cells to incorporate bromodeoxyuridine was investigated. From the results of these studies, we conclude that SVZa cells in the RMS can successively down‐regulate their expression of p19INK4d as they migrate and that they repeatedly exit and reenter the cell cycle while en route to the olfactory bulb. These studies led us to investigate whether bone morphogenetic proteins (BMPs) are involved in the regulation of SVZa cell proliferation and p19INK4d expression, because, elsewhere in the CNS, BMPs modulate cell proliferation and influence cell fate decisions. To determine the effects of BMP signaling on SVZa cell proliferation and differentiation, we altered the expression of the BMP receptor Ia (BMPR‐Ia) using retrovirally mediated gene transfer. The cells in the SVZa encoding the wild‐type BMPR‐Ia exit the cell cycle and do not appear to migrate through the RMS. Conversely, both within the SVZa and along the RMS, the majority of SVZa‐derived cells encoding a dominant‐negative BMPR‐Ia gene do not express p19INK4d. These findings indicate that p19INK4d expression is suppressed when BMP signaling is inhibited. Furthermore, SVZa‐derived cells with both augmented and inhibited BMP signaling retain their neuronal commitment. Collectively, these studies have revealed that SVZa cell proliferation and differentiation is under the control of several interacting intrinsic and extrinsic factors. © 2002 Wiley‐Liss, Inc.

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“…These variabilities might be explained not only by the pooling of all proliferating V-SVZ cells but also because these previous studies are based on the analysis of tissue sections. Neuroblasts continue to divide as they actively migrate tangentially (5,15). Therefore, dividing cells move in and out of the counting bin in coronal or sagittal sections, likely introducing errors in the analysis (16).…”

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confidence: 99%