TU Darmstadt / ULB / TUbiblio

Regulation of the rat oligodendroglia cell line OLN-93 by antisense transfection of butyrylcholinesterase.

Robitzki, A. ; Döll, F. ; Richter-Landsberg, C. ; Layer, Paul G. (2000)
Regulation of the rat oligodendroglia cell line OLN-93 by antisense transfection of butyrylcholinesterase.
In: Glia, 31 (3)
Artikel, Bibliographie

Kurzbeschreibung (Abstract)

Butyrylcholinesterase (BChE) is a glial cell marker with unknown function. For neuroepithelial cells, BChE has been shown to regulate cell division and expression of the postmitotic marker acetylcholinesterase (AChE), while similar studies are lacking for glial cells. By transducing an antisense-5'BChE cDNA expression vector via calcium phosphate precipitation, we have analyzed the effect of BChE inhibition on proliferation and differentiation of rat oligodendroglia-derived OLN-93 cells. OLN-93 cells were chosen because they are highly proliferative, while expressing markers of differentiated oligodendrocytes (Richter-Landsberg and Heinrich, 1996). First, we established that OLN-93 cells do express BChE protein, albeit chiefly in an inactive state, and that BChE was decreased by antisense-5'BChE transfection. Cell proliferation was also strongly diminished, protein kinase C (PKCalpha) was upregulated, and expression of cytoskeletal and cell surface proteins was altered. In particular, immunoreactivities of the intermediate filament proteins vimentin and the cell adhesion protein F11 were detected, indicating that BChE-inhibited OLN-93 cells have shifted toward an astrocytic phenotype. These data support a role of the glia marker BChE in CNS glial cell proliferation and differentiation, achieved via a nonenzymatic mechanism. The possible biomedical impact of BChE protein, e.g., on CNS nerve regeneration, is briefly discussed.

Typ des Eintrags: Artikel
Erschienen: 2000
Autor(en): Robitzki, A. ; Döll, F. ; Richter-Landsberg, C. ; Layer, Paul G.
Art des Eintrags: Bibliographie
Titel: Regulation of the rat oligodendroglia cell line OLN-93 by antisense transfection of butyrylcholinesterase.
Sprache: Englisch
Publikationsjahr: 2000
Titel der Zeitschrift, Zeitung oder Schriftenreihe: Glia
Jahrgang/Volume einer Zeitschrift: 31
(Heft-)Nummer: 3
Kurzbeschreibung (Abstract):

Butyrylcholinesterase (BChE) is a glial cell marker with unknown function. For neuroepithelial cells, BChE has been shown to regulate cell division and expression of the postmitotic marker acetylcholinesterase (AChE), while similar studies are lacking for glial cells. By transducing an antisense-5'BChE cDNA expression vector via calcium phosphate precipitation, we have analyzed the effect of BChE inhibition on proliferation and differentiation of rat oligodendroglia-derived OLN-93 cells. OLN-93 cells were chosen because they are highly proliferative, while expressing markers of differentiated oligodendrocytes (Richter-Landsberg and Heinrich, 1996). First, we established that OLN-93 cells do express BChE protein, albeit chiefly in an inactive state, and that BChE was decreased by antisense-5'BChE transfection. Cell proliferation was also strongly diminished, protein kinase C (PKCalpha) was upregulated, and expression of cytoskeletal and cell surface proteins was altered. In particular, immunoreactivities of the intermediate filament proteins vimentin and the cell adhesion protein F11 were detected, indicating that BChE-inhibited OLN-93 cells have shifted toward an astrocytic phenotype. These data support a role of the glia marker BChE in CNS glial cell proliferation and differentiation, achieved via a nonenzymatic mechanism. The possible biomedical impact of BChE protein, e.g., on CNS nerve regeneration, is briefly discussed.

Fachbereich(e)/-gebiet(e): 10 Fachbereich Biologie
?? fb10_zoologie ??
10 Fachbereich Biologie > Developmental Biology and Neurogenetics
Hinterlegungsdatum: 21 Nov 2011 14:26
Letzte Änderung: 05 Mär 2013 09:56
PPN:
Export:
Suche nach Titel in: TUfind oder in Google
Frage zum Eintrag Frage zum Eintrag

Optionen (nur für Redakteure)
Redaktionelle Details anzeigen Redaktionelle Details anzeigen