Wnt-1 inhibits nerve growth factor-induced differentiation of PC12 cells by preventing the induction of some but not all late-response genes

Chou, Alice H; Zheng, Shuang; Itsukaichi, Tomoko; Howard, Bruce D.

doi:10.1016/s0169-328x(00)00058-9

Cited by 37 publications

(18 citation statements)

References 43 publications

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“…These findings support a D1 receptor-mediated striatal influence on cortical activity. Similarly, the D1 receptor antagonist-induced lack of SCG10 and GAP-43 upregulation reported here may reflect attenuated systemic activation (Stein et al, 1988b,Sheng and Greenberg, 1990,Chou et al, 2000.…”

Section: Discussionmentioning

confidence: 54%

Intrastriatal dopamine D1 antagonism dampens neural plasticity in response to motor cortex lesion

2007

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Motor cortex lesions in rats partially denervate the striatum, producing behavioral deficits and inducing reactive neuroplasticity. Plastic responses include changes in growth-associated protein marker expression and anatomical restructuring. Corticostriatal plasticity is dependent on dopamine at the striatal target, where D1 receptor signaling reinforces behaviorally relevant neural activity. To determine whether striatal dopamine D1 receptor signaling is important for the growth-associated protein responses and behavioral recovery that follow unilateral motor cortex aspiration, the dopamine D1 receptor antagonist SCH23390 was intrastriatally infused in cortically lesioned animals. After a cortical aspiration lesion in Long Evans rats, the growth-associated proteins SCG10 and GAP-43 were upregulated in the cortex contralateral to the lesion at 30 days post-lesion. However, continuous unilateral intrastriatal infusion of SCH23390 prevented this aspiration-induced upregulation. Furthermore, lesioned rats demonstrated spontaneous sensorimotor improvement, in terms of limb-use symmetry, about one month post-lesion. This improvement was prevented with chronic intrastriatal SCH23390 infusion. The D1 receptor influence may be important to normalize corticostriatal activity (and observable behavior), either in a long-term manner or temporarily until other more permanent means of synaptic regulation, such as sprouting or synaptogenesis, may be implemented. Keywords cortical ablation; striatum; SCH23390The ability to reorganize neural connections according to changing environmental cues is essential to the formation of the wide network of limbic, striatal, and cortical circuits that regulate the complex array of human behaviors. Generally referred to as neural plasticity, these adaptive processes are most obvious in the developing brain, but are also utilized throughout adulthood as new skills and memories are acquired. Likewise, when the brain is damaged by trauma or disease, adaptive mechanisms of plasticity are brought into play and are critical for determining the limits of functional recovery (Ivanco and Greenough, 2000,Johansson, 2000,Nudo et al., 2001,Gonzalez and Kolb, 2003. These adaptive processes are governed by local extra-and intracellular signals and can be manipulated by various experimental interventions including: exercise (Cotman and Berchtold, 2002,Gomez-Pinilla et al., 2002) Tel: 323-442-2126; Fax: 323-442-2127. E-mail address: elizabjd@usc.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (van Praag et al., 2000), motor skills training (Plautz et a...

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Section: Discussionmentioning

confidence: 54%

Intrastriatal dopamine D1 antagonism dampens neural plasticity in response to motor cortex lesion

2007

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“…Optimedin's action on stimulated PC12 cells in some respects resembles action of Wnt proteins [25][26][27][28]. Similar to optimedin expression, expression of Wnt1 or Wnt3a cDNAs in PC12 cells inhibited NGF-induced differentiation PC12 cells and neurite growth.…”

Section: Optimedin Does Not Stimulate Tcf/lef Signalingmentioning

confidence: 86%

“…Optimedin, similar to some other secreted glycoproteins, may interact with cellular receptor(s) and stimulates or inhibits cellular signaling pathways. Altough optimedin's action on stimulated PC12 cells in some respects resembles action of Wnt proteins [25][26][27][28], optimedin does not stimulate the canonical Wnt pathway through TCF/LEF signaling (Fig. 5).…”

Section: Discussionmentioning

confidence: 99%

“…Similar to optimedin expression, expression of Wnt1 or Wnt3a cDNAs in PC12 cells inhibited NGF-induced differentiation PC12 cells and neurite growth. Similar to optimedin, expression of Wnt1 increased the rate of multiplication of PC12 cells [26] and increased calcium-dependent cellular adhesion. Therefore, we examined whether optimedin may activate the Wnt canonical signaling pathway using Wnt-responsive TOPFlash luciferase reporter and HEK293 cells which are often used to study Wnt signaling.…”

Section: Optimedin Does Not Stimulate Tcf/lef Signalingmentioning

confidence: 90%

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Optimedin induces expression of N-cadherin and stimulates aggregation of NGF-stimulated PC12 cells

Lee

Tomarev

2007

Experimental Cell Research

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Optimedin, also known as olfactomedin 3, belongs to a family of olfactomedin domain-containing proteins. It is expressed in neural tissues and Pax6 is involved in the regulation of its promoter. To study possible effects of optimedin on the differentiation of neural cells, we produced stably transfected PC12 cell lines expressing optimedin under a tetracycline-inducible promoter. Cells expressing high levels of optimedin showed higher growth rates and stronger adhesion to the collagen extracellular matrix as compared with control PC12 cells. After stimulation with nerve growth factor (NGF), optimedin-expressing cells demonstrated elevated levels of N-cadherin, β-catenin, α-catenin, and occludin as compared with stimulated, control PC12 cells. Expression of optimedin induced Ca 2+ -dependent aggregation of NGF-stimulated PC12 cells and this aggregation was blocked by the expression of N-cadherin siRNA. Expression of optimedin also changed the organization of the actin cytoskeleton and inhibited neurite outgrowth in NGF-stimulated PC12 cells. We suggest that expression of optimedin stimulates the formation of adherent and tight junctions on the cell surface and this may play an important role in the differentiation of the brain and retina through the modulation of cytoskeleton organization, cell-cell adhesion and migration.

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“…The TopFlash/FopFlash assay for Lef-1/Tcf activity was performed as described by Korinek et al (1997) with the variations described by Chou et al (2000). b-galactosidase was assayed as described (Sambrook et al, 1989).…”

Section: Topflash/fopflash Assay For Lef-1/tcf Activitymentioning

confidence: 99%

Inhibition by Wnt-1 or Wnt-3a of nerve growth factor-induced differentiation of PC12 cells is reversed by bisindolylmaleimide-I but not by several other PKC inhibitors

Chou

Howard

2002

Oncogene

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Wnt-1 and Wnt-3a exhibit redundancy in neural crest development. We have found that they do not produce the same effects on PC12 cells, which were obtained from the adrenal medulla, a neural crest derivative. However, both Wnt-1 or Wnt-3a inhibit nerve growth factor (NGF)-induced neurite outgrowth. The inhibition is reversed by the protein kinase C (PKC) inhibitor, bisindolylmaleimide-I, but it did not reverse Wnt-1-induced activation of the canonical Wnt pathway. The Wnt-1 inhibitory effect was not reversed by several other PKC inhibitors, by phorbol ester-induced down-regulation of PKC, or by pertussis toxin, which is known to inhibit another Wnt signaling pathway, the Wnt/Ca 2+ pathway. We suggest that bisindolylmaleimide-I acts by affecting either a pathway downstream from Lef-1/Tcf in the canonical pathway or a Wnt signaling pathway other than the canonical pathway. In either case, the bisindolylmaleimide-I sensitivity of this pathway should aid in its identification.

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Wnt-1 inhibits nerve growth factor-induced differentiation of PC12 cells by preventing the induction of some but not all late-response genes

Cited by 37 publications

References 43 publications

Intrastriatal dopamine D1 antagonism dampens neural plasticity in response to motor cortex lesion

Intrastriatal dopamine D1 antagonism dampens neural plasticity in response to motor cortex lesion

Optimedin induces expression of N-cadherin and stimulates aggregation of NGF-stimulated PC12 cells

Inhibition by Wnt-1 or Wnt-3a of nerve growth factor-induced differentiation of PC12 cells is reversed by bisindolylmaleimide-I but not by several other PKC inhibitors

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