TY - JOUR
T1 - 1-40 β-amyloid protein fragment modulates the expression of CD44 and CD71 on the astrocytoma cell line in the presence of IL1β and TNFα
AU - Speciale, Livianna
AU - Ruzzante, Stefania
AU - Calabrese, Elena
AU - Saresella, Marina
AU - Taramelli, Donatella
AU - Mariani, Claudio
AU - Bava, Laura
AU - Longhi, Renato
AU - Ferrante, Pasquale
PY - 2003/7/1
Y1 - 2003/7/1
N2 - 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-1β (IL1β), tumour necrosis factor-α (TNFα) and 1-40 or 25-35 β-amyloid (Aβ) fragments. The percentage of 1321N1 astrocytoma cell line expressing these markers increased significantly after treatment with TNFα or IL1β. The presence of Aβ 1-40 fragment, alone or in combination with IL1β, induced an increase in the percentage of cells expressing CD44, but not VCAM-1. However, the concomitant presence of Aβ 1-40 fragment and of IL1β or TNFα caused an increase in the percentage of CD71 positive cells. In contrast, the shorter Aβ 25-35 fragment was always inactive. These results indicates that Aβ 1-40 fragment, in association with cytokines, can activate this astrocyte-derived cell line and add further elements in favour of the hypothesis that β-amyloid can act as immunological mediator.
AB - 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-1β (IL1β), tumour necrosis factor-α (TNFα) and 1-40 or 25-35 β-amyloid (Aβ) fragments. The percentage of 1321N1 astrocytoma cell line expressing these markers increased significantly after treatment with TNFα or IL1β. The presence of Aβ 1-40 fragment, alone or in combination with IL1β, induced an increase in the percentage of cells expressing CD44, but not VCAM-1. However, the concomitant presence of Aβ 1-40 fragment and of IL1β or TNFα caused an increase in the percentage of CD71 positive cells. In contrast, the shorter Aβ 25-35 fragment was always inactive. These results indicates that Aβ 1-40 fragment, in association with cytokines, can activate this astrocyte-derived cell line and add further elements in favour of the hypothesis that β-amyloid can act as immunological mediator.
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U2 - 10.1002/jcp.10295
DO - 10.1002/jcp.10295
M3 - Article
C2 - 12767055
AN - SCOPUS:0037945813
VL - 196
SP - 190
EP - 195
JO - Journal of cellular and comparative physiology
JF - Journal of cellular and comparative physiology
SN - 0021-9541
IS - 1
ER -