Browse

Transforming growth factor b1 regulates the fate of cultured spinal cord-derived neural progenitor cells.

DC Field Value Language
dc.contributor.authorPark, S. M-
dc.contributor.authorJung, J. S-
dc.contributor.authorJang, M. S-
dc.contributor.authorKang, K. S-
dc.contributor.authorKang, S. K-
dc.date.accessioned2010-08-03T23:23:13Z-
dc.date.available2010-08-03T23:23:13Z-
dc.date.issued2008-03-
dc.identifier.citationCell Proliferation 41, 248-264en
dc.identifier.issn0960-7722-
dc.identifier.urihttps://hdl.handle.net/10371/68906-
dc.description.abstractObjectives: We have evaluated the physiological roles of transforming growth factor-β1 (TGF-β1) on differentiation, migration, proliferation and anti-apoptosis characteristics of cultured spinal cord-derived neural progenitor cells. Methods: We have used neural progenitor cells that had been isolated and cultured from mouse spinal cord tissue, and we also assessed the relevant reaction mechanisms using an activin-like kinase (ALK)-specific inhibitory system including an inhibitory RNA, and found that it involved potential signalling molecules such as phosphatidylinositol-3-OH kinase (PI3K)/Akt and mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK1/2). Results and Conclusions: Transforming growth factor-β1-mediated cell population growth was activated after treatment and was also effectively blocked by an ALK41517-synthetic inhibitor (4-(5-benzo(1,3) dioxol-5-yl-4-pyridine-2-yl-1H-imidazole-2-yl) benzamide (SB431542) and ALK siRNA, thereby indicating the involvement of SMAD2 in the TGF-β1-mediated growth and migration of these neural progenitors cells (NPC). In the present study, TGF-β1 actively induced NPC migration in vitro. Furthermore, TGF-β1 demonstrated extreme anti-apoptotic behaviour against hydrogen peroxide-mediated apoptotic cell death. At low dosages, TGF-β1 enhanced (by approximately 76%) cell survival against hydrogen peroxide treatment via inactivation of caspase-3 and -9. TGF-β1-treated NPCs down-regulated Bax expression and cytochrome c release; in addition, the cells showed up-regulated Bcl-2 and thioredoxin reductase 1. They also had increased p38, Akt and ERK1/2 phosphorylation, showing the involvement of both the PI3K/Akt and MAPK/ERK1/2 pathways in the neuroprotective effects of TGF-β1. Interestingly, these effects operate on specific subtypes of cells, including neurones, neural progenitor cells and astrocytes in cultured spinal cord tissue-derived cells. Lesion sites of spinal cord-overexpressing TGF-β1-mediated prevention of cell death, cell growth and migration enhancement activity have been introduced as a possible new basis for therapeutic strategy in treatment of neurodegenerative disorders, including spinal cord injuries.en
dc.language.isoenen
dc.publisherWiley-Blackwellen
dc.titleTransforming growth factor b1 regulates the fate of cultured spinal cord-derived neural progenitor cells.en
dc.typeArticleen
dc.identifier.doi10.1111/j.1365-2184.2008.00514.x-
Appears in Collections:
College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
Files in This Item:
There are no files associated with this item.
  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse