Abstract:
:Neural progenitor cells isolated from the embryonic cerebral cortex are well known to differentiate into neurons and glial cells, but recent reports have demonstrated differentiation into smooth muscle cells (SMCs) under the influence of fetal bovine serum. In this study, we report that agonists for G protein-coupled receptors (GPCRs), including endothelin, lysophosphatidic acid and carbachol, effectively promote the expression of SMC-specific proteins in the presence of transforming growth factor-beta (TGF-beta). Incubation of neural progenitor cells with agonists for GPCRs or TGF-beta alone induced the expression of an SMC-specific protein, alpha-smooth muscle actin (SMA), and their combination resulted in incremental increase. Stimulation with combinations of each GPCR agonist and TGF-beta increased the numbers of large, flat cells with thick actin fibers and also caused expression of other SMC marker proteins. Endothelin and TGF-beta enhanced SMA promoter-luciferase reporter activity at different times after stimulation. The mutation of TGF-beta control element of SMA promoter constructs decreased TGF-beta-enhanced luciferase activity but not endothelin-stimulated activity. Transfection of active forms of RhoA and its effector, mDia, strongly enhanced SMA promoter activity, and a dominant negative form of RhoA inhibited endothelin-stimulated promoter activity but not TGF-beta-stimulated activity. Whereas endothelin consistently activated RhoA, TGF-beta did not, and a specific inhibitor of TGF-beta type I receptor blocked TGF-beta-enhanced SMA promoter activity, suggesting involvement of Smad phosphorylation. These results suggest that separate signaling pathways of G protein and TGF-beta cooperatively promote the expression of SMC-specific proteins in neural progenitor cells.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Morishita R,Nagata K,Ito H,Ueda H,Asano M,Shinohara H,Kato K,Asano Tdoi
10.1111/j.1471-4159.2006.04405.xsubject
Has Abstractpub_date
2007-05-01 00:00:00pages
1031-40issue
4eissn
0022-3042issn
1471-4159pii
JNC4405journal_volume
101pub_type
杂志文章abstract::Activation of metabotropic glutamate receptors (mGluRs) in glia results in significant physiological effects for both the glia and the neighboring neurons; but in many cases, the mGluR subtypes and signal transduction mechanisms mediating these effects have not been determined. In this study, we report that mGluR acti...
journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
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pub_type: 杂志文章
doi:10.1111/j.1471-4159.1985.tb05502.x
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1992.tb08453.x
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1111/j.1471-4159.1992.tb09276.x
更新日期:1992-01-01 00:00:00
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1111/j.1471-4159.1984.tb00920.x
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
doi:10.1046/j.1471-4159.1999.0720491.x
更新日期:1999-02-01 00:00:00
abstract::Astrogliosis occurs after brain ischemia, and excessive astrogliosis can devastate the neuronal recovery. Previous reports show that galectin-1 (Gal-1) regulates proliferation of several cell types and plays an important role after nervous system injuries. Here, we found that expression of Gal-1 was remarkably up-regu...
journal_title:Journal of neurochemistry
pub_type: 杂志文章
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更新日期:2011-01-01 00:00:00
abstract::Exposure to cocaine-associated conditioned stimuli elicits craving and increases the probability of cocaine relapse in cocaine users even after extended periods of abstinence. Recent evidence indicates that cocaine seeking can be inhibited by disrupting the reconsolidation of the cocaine cue memories and that basolate...
journal_title:Journal of neurochemistry
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更新日期:2011-07-01 00:00:00