In vivo regulation of precursor cells in the subventricular zone of adult rat brain by thyroid hormone and retinoids

Giardino, Luciana; Bettelli, Carla; Calzà, Laura

doi:10.1016/s0304-3940(00)01580-9

Cited by 23 publications

(17 citation statements)

References 17 publications

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“…Moreover, in SVZ neurosphere stem cell and parasagittal brain slice cultures derived from postnatal mouse, RA exposure increased neurogenesis by enhancing the proliferation and neuronal differentiation of forebrain SVZ neuroblasts (Wang et al, 2005). Furthermore, prolonged oral RA administration also increases adult rat SVZ cell proliferation (Giardino et al, 2000). However, opposite effects of RA were also reported.…”

Section: Discussionmentioning

confidence: 99%

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Effects of retinoic acid on ischemic brain injury-induced neurogenesis

Jung

Baek²,

Park³

et al. 2007

Exp Mol Med

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Neurogenesis can be induced by pathological conditions such as cerebral ischemia. However the molecular mechanisms or modulating reagents of the reactive neurogenesis after the cerebral ischemia are poorly characterized. Retinoic acid (RA) has been shown to increase neurogenesis by enhancing the proliferation and neuronal differentiation of forebrain neuroblasts. Here, we examined whether RA can modulate the reactive neurogenesis after the cerebral ischemia. In contrast to our expectation, RA treatment decreased the reactive neurogenesis in subventricular zone (SVZ), subgranular zone (SGZ) and penumbral region. Furthermore, RA treatment also decreased the angiogenesis and gliosis in penumbral region.

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Section: Discussionmentioning

confidence: 99%

“…RA exposure stimulates neurogenesis in neural stem cell cultures isolated from the embryonic striatal SVZ or adult hippocampus (Wohl and Weiss, 1998;Wang et al, 2005). Moreover, prolonged oral RA administration also increases adult rat SVZ cell proliferation (Giardino et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Effects of retinoic acid on ischemic brain injury-induced neurogenesis

Jung

Baek²,

Park³

et al. 2007

Exp Mol Med

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“…However, the high correlation between changes in neurosphere size and changes in self-renewal suggests that a common mechanism underlies both of these effects. In order to test for a direct effect of p21 loss on progenitor cell populations, we examined the expression of the endogenous proliferation marker, Ki67 (Giardino et al 2000;Enwere et al 2004), in the adult subependyma of the lateral ventricle of p21 −/− and p21 +/+ mice at 60 d and 480 d of age. In contrast with the effect of p21 loss on NSC number, there was no effect of p21 loss on the number of Ki67-labeled cells in 60-d mice, but there was a significantly greater age-related reduction in the number of Ki67-labeled cells in p21 −/− compared to p21 +/+ mice at 480 d (Fig.…”

Section: Loss Of P21 Does Not Directly Affect Nsc Progeny In Vivo Bumentioning

confidence: 99%

p21 loss compromises the relative quiescence of forebrain stem cell proliferation leading to exhaustion of their proliferation capacity

Kippin

Martens²,

Kooy³

2005

Genes Dev.

390

357

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“…RA exposure stimulates neurogenesis in neural stem cell cultures isolated from the embryonic striatal SVZ or adult hippocampus (Wohl and Weiss, 1998;Takahashi et al, 1999). Prolonged oral RA administration also increases adult rat SVZ cell proliferation (Giardino et al, 2000). Moreover, the lateral ganglionic eminence (LGE), which gives rise to the striatum under the influence of RA, evolves into the postnatal forebrain SVZ and is a source of olfactory bulb neurons (Anderson et al, 1997;Wichterle et al, 1999;Toresson and Campbell, 2001;Stenman et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Retinoic acid regulates postnatal neurogenesis in the murine subventricular zone-olfactory bulb pathway

2005

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Neurogenesis persists throughout life in the rodent subventricular zone (SVZ)-olfactory bulb pathway. The molecular regulation of this neurogenic circuit is poorly understood. Because the components for retinoid signaling are present in this pathway, we examined the influence of retinoic acid (RA) on postnatal SVZ-olfactory bulb neurogenesis. Using both SVZ neurosphere stem cell and parasagittal brain slice cultures derived from postnatal mouse, we found that RA exposure increased neurogenesis by enhancing the proliferation and neuronal differentiation of forebrain SVZ neuroblasts. The RA precursor retinol had a similar effect, which was reversed by treating cultures with the RA synthesis inhibitor disulfiram. Electroporation of dominant-negative retinoid receptors into the SVZ of slice cultures also blocked neuroblast migration to the olfactory bulb and altered the morphology of the progenitors. Moreover, the administration of disulfiram to neonatal mice decreased in vivo cell proliferation in the striatal SVZ. These results indicate that RA is a potent mitogen for SVZ neuroblasts and is required for their migration to the olfactory bulb. The regulation of multiple steps in the SVZ-olfactory bulb neurogenic pathway by RA suggests that manipulation of retinoid signaling is a potential therapeutic strategy to augment neurogenesis after brain injury.

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In vivo regulation of precursor cells in the subventricular zone of adult rat brain by thyroid hormone and retinoids

Cited by 23 publications

References 17 publications

Effects of retinoic acid on ischemic brain injury-induced neurogenesis

Effects of retinoic acid on ischemic brain injury-induced neurogenesis

p21 loss compromises the relative quiescence of forebrain stem cell proliferation leading to exhaustion of their proliferation capacity

Retinoic acid regulates postnatal neurogenesis in the murine subventricular zone-olfactory bulb pathway

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