The modulation of CD44, VCAM-1 and CD71 expression was analysed by flow cytometry in the 1321N1 astrocytoma cell line in the presence of interleukin-1beta (IL1beta), tumour necrosis factor-alpha (TNFalpha) and 1-40 or 25-35 beta-amyloid (Abeta) fragments. The percentage of 1321N1 astrocytoma cell line expressing these markers increased significantly after treatment with TNFalpha or IL1beta. The presence of Abeta 1-40 fragment, alone or in combination with IL1beta, induced an increase in the percentage of cells expressing CD44, but not VCAM-1. However, the concomitant presence of Abeta 1-40 fragment and of IL1beta or TNFalpha caused an increase in the percentage of CD71 positive cells. In contrast, the shorter Abeta 25-35 fragment was always inactive. These results indicates that Abeta 1-40 fragment, in association with cytokines, can activate this astrocyte-derived cell line and add further elements in favour of the hypothesis that beta-amyloid can act as immunological mediator.

1-40 Beta-amyloid protein fragment modulates the expression of CD44 and CD71 on the astrocytoma cell line in the presence of IL1beta and TNFalpha / L. Speciale, S. Ruzzante, E. Calabrese, M. Saresella, D. Taramelli, C. Mariani, L. Bava, R. Longhi, P. Ferrante. - In: JOURNAL OF CELLULAR PHYSIOLOGY. - ISSN 0021-9541. - 196:1(2003 Jul), pp. 190-195.

1-40 Beta-amyloid protein fragment modulates the expression of CD44 and CD71 on the astrocytoma cell line in the presence of IL1beta and TNFalpha

D. Taramelli;C. Mariani;P. Ferrante
2003

Abstract

The modulation of CD44, VCAM-1 and CD71 expression was analysed by flow cytometry in the 1321N1 astrocytoma cell line in the presence of interleukin-1beta (IL1beta), tumour necrosis factor-alpha (TNFalpha) and 1-40 or 25-35 beta-amyloid (Abeta) fragments. The percentage of 1321N1 astrocytoma cell line expressing these markers increased significantly after treatment with TNFalpha or IL1beta. The presence of Abeta 1-40 fragment, alone or in combination with IL1beta, induced an increase in the percentage of cells expressing CD44, but not VCAM-1. However, the concomitant presence of Abeta 1-40 fragment and of IL1beta or TNFalpha caused an increase in the percentage of CD71 positive cells. In contrast, the shorter Abeta 25-35 fragment was always inactive. These results indicates that Abeta 1-40 fragment, in association with cytokines, can activate this astrocyte-derived cell line and add further elements in favour of the hypothesis that beta-amyloid can act as immunological mediator.
Alzheimers-disease; transferrin receptors; senile plaques; brain; precursor; secretion; peptide; inhibition; sulfate; IL-6
Settore MED/04 - Patologia Generale
Settore MED/07 - Microbiologia e Microbiologia Clinica
lug-2003
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/201145
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