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P4‐189: ABVAC40 TREATMENT IN DOGS INDUCES SPECIFIC ANTIBODY RESPONSE AND INCREMENT OF Aβ40 LEVELS IN PLASMA
Author(s) -
Lacosta Ana M.,
Fandos Noelia,
Pérez-Grijalba Virginia,
Pesini Pedro,
Sarasa Manuel
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.06.2594
Subject(s) - placebo , antibody , immunogenicity , medicine , context (archaeology) , vaccination , titer , immunology , antibody titer , gastroenterology , biology , pathology , paleontology , alternative medicine
colocalized with LRP1 in SH-SY5Y cells. The MAPKs (P38, JNK, ERK) were activated (P<0.05), the expression level of LRP1 (P<0.01) were also significantly increased, compared to the saline group, while the SH-SY5Y cells were treated with Ab1-42. By using the p38 MAPK inhibitor SB202190, the expression of LRP1 level significantly decreased (P<0.05). ERK1/2 MAPK inhibitor decreases the level of LRP1 (P<0.01) expression. However, in JNK MAPK inhibitor treated group, the level of LRP1 (P<0.05) significantly increased. In the study of Ab induced toxicity, Ab (5 mM, 18 h) up-regulates the expression of Bcl2/Bax (P<0.05), and increases the Cyt c (P<0.01) release. The p38, ERK1/2 MAPK inhibitor could up-regulate the Bcl2/Bax (P<0.05) level, decrease the level of Cyt c (P<0.05) release. JNK MAPK inhibitor has no significant effects on the level of Bcl2/Bax and Cyt c. Conclusions: Exogenous Ab could be internalized by SH-SY5Y cells; MAPK signaling pathways were activated by Ab; The MAPK signaling pathways could regulate the Ab level through the LRP1; Ab was internalized and could induce toxic effect on SH-SY5Y cells.