Platelet-derived growth factor induces chemotaxis of neuroepithelial stem cells

Forsberg-Nilsson, Karin; Behar, Toby; Afrakhte, Mozhgan; Barker, Jeffery L.; McKay, Ronald D.G.

doi:10.1002/(sici)1097-4547(19980901)53:5<521::aid-jnr2>3.0.co;2-b

Cited by 67 publications

(29 citation statements)

References 45 publications

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“…PDGFR␣ expression is found in neural stem cells and is a characteristic of this stem cell type (33,34). Expression of PDGFR␣ was observed in the isolated LHR-negative-PDGFR␣-positive cells, corroborating an increasing body of evidence that PDGF signaling is necessary for stem cell commitment and differentiation in the LC lineage of mice and neonatal rats (35,36).…”

Section: Discussionsupporting

confidence: 66%

In search of rat stem Leydig cells: Identification, isolation, and lineage-specific development

Dong

Sottas

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

240

301

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Leydig cells (LCs) are thought to differentiate from spindle-shaped precursor cells that exhibit some aspects of differentiated function, including 3␤-hydroxysteroid dehydrogenase (3␤HSD) activity. The precursor cells ultimately derive from undifferentiated stem LCs (SLCs), which are postulated to be present in testes before the onset of precursor cell differentiation. We searched for cells in the neonatal rat testis with the abilities to: (i) proliferate and expand indefinitely in vitro (self renew); (ii) differentiate (i.e., 3␤HSD and ultimately synthesize testosterone); and (iii) when transplanted into host rat testes, colonize the interstitium and subsequently differentiate in vivo. At 1 week postpartum, spindle-shaped cells were seen in the testicular interstitium that differed from the precursor cells in that they were 3␤HSD-negative, luteinizing hormone (LH) receptor (LHR)-negative, and platelet-derived growth factor receptor ␣ (PDGFR␣)-positive. These cells were purified from the testes of 1-week-old rats. The cells contained proteins known to be involved in LC development, including GATA4, c-kit receptor, and leukemia inhibitory factor receptor. The putative SLCs expanded over the course of 6 months while remaining undifferentiated. When treated in media that contained thyroid hormone, insulin-like growth factor I, and LH, 40% of the putative SLCs came to express 3␤HSD and to synthesize testosterone. When transplanted into host rat testes from which LCs had been eliminated, the putative SLCs colonized the interstitium and subsequently expressed 3␤HSD, demonstrating their ability to differentiate in vivo. We conclude that these cells are likely to be the sought-after SLCs.c-kit ͉ leukemia inhibitory factor ͉ platelet-derived growth factor receptor ␣ ͉ puberty ͉ steroidogenesis L eydig cells (LCs) are the primary source of testosterone in the male, and their differentiation in the testes during puberty is a signature event in the development of the male body plan. It is hypothesized, but far from proven, that LCs first arise from undifferentiated stem cells [stem LCs (SLCs)] (1-3). It has been suggested that, in rats, the putative SLCs are present in the testis at birth, and that by 11 days postpartum, at least some of their progeny express LC-specific genes and thus become committed to the LC lineage (4, 5).The committed cells subsequently undergo phased transitions through progenitor and immature stages and ultimately to terminally differentiated adult LC stage (6). In particular, progenitor LCs (PLCs) form during days 12-28 postpartum (presumably from SLCs). The PLCs proliferate and also exhibit some aspects of differentiated function, including 3␤-hydroxysteroid dehydrogenase (3␤HSD) activity (7). Luteinizing hormone (LH) receptors (LHRs) first appear as the PLCs differentiate, suggesting that SLCs are likely to be independent of LH control (8). The development of the steroidogenic capacity of PLCs requires stimulation by LH (9). The mitotic activity of PLCs gradually is reduced, and the cells enlarge...

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Section: Discussionsupporting

confidence: 66%

In search of rat stem Leydig cells: Identification, isolation, and lineage-specific development

Dong

Sottas

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

240

301

View full text Add to dashboard Cite

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“…Although PDGF's role in smooth muscle cell, fibroblast, and oligodendrocyte migration is well established (Wolswijk et al 1991;Bilato et al 1995;Milner et al 1997;Facchiano et al 2000), its role in modulating astrocyte migration is less well defined and therefore merits further investigation. Indeed, cell culture studies have revealed the capacity of PDGF to stimulate migration of oligodendrocyte progenitor cells (Simpson and Armstrong 1999), neonatal rat cortical astrocytes (Bressler et al 1985), and embryonic rat neural stem cells (Forsberg-Nilsson et al 1998). In cell culture-based studies, PDGF, in combination with bFGF, has been shown to promote proliferation of glial progenitors and inhibit their terminal differentiation (McKinnon et al 1990).…”

Section: The Glioma-relevant Pathwaysmentioning

confidence: 99%

Malignant glioma: genetics and biology of a grave matter

Maher¹,

Furnari²,

et al. 2001

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“…The discovery of netrins (18)(19)(20)(21), semaphorins (22)(23)(24), ephrins (25,26), and Slit proteins (27)(28)(29) established the existence of neuronal migration guidance signals at long distances by diffusible secreted proteins that have NSPC chemoattractant and repulsive properties. Recently it has been suggested that certain cytokines with known important functions in CNS development (i.e., transforming growth factor α, bFGF, and EGF) were capable of enhancing ischemia-induced progenitor proliferation and migration (30,31). Nevertheless, our understanding of the mechanisms guiding neural progenitor cell migration in pathological states remains limited.…”

Section: Introductionmentioning

confidence: 99%

Neuronally expressed stem cell factor induces neural stem cell migration to areas of brain injury

Sun¹,

Lee²,

Fine³

2004

J. Clin. Invest.

204

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Neural stem/progenitor cell (NSPC) migration toward sites of damaged central nervous system (CNS) tissue may represent an adaptive response for the purpose of limiting and/or repairing damage. Little is known of the mechanisms responsible for this migratory response. We constructed a cDNA library of injured mouse forebrain using subtractive suppression hybridization (SSH) to identify genes that were selectively upregulated in the injured hemisphere. We demonstrate that stem cell factor (SCF) mRNA and protein are highly induced in neurons within the zone of injured brain. Additionally, the SCF receptor c-kit is expressed on NSPCs in vitro and in vivo. Finally, we demonstrate that recombinant SCF induces potent NSPC migration in vitro and in vivo through the activation of c-kit on NSPCs. These data suggest that the SCF/c-kit pathway is involved in the migration of NSPCs to sites of brain injury and that SCF may prove useful for inducing progenitor cell recruitment to specific areas of the CNS for cell-based therapeutic strategies.

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Platelet-derived growth factor induces chemotaxis of neuroepithelial stem cells

Cited by 67 publications

References 45 publications

In search of rat stem Leydig cells: Identification, isolation, and lineage-specific development

In search of rat stem Leydig cells: Identification, isolation, and lineage-specific development

Malignant glioma: genetics and biology of a grave matter

Neuronally expressed stem cell factor induces neural stem cell migration to areas of brain injury

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