The Complexity of Sporadic Alzheimer’s Disease Pathogenesis: The Role of RAGE as Therapeutic Target to Promote Neuroprotection by Inhibiting Neurovascular Dysfunction
Figure 2
Aβ induces RAGE-dependent TXNIP expression in RBE4 brain endothelial cells. RBE4 cells were maintained 5 days in differentiation medium (F10/MEM, 2.5% FCS, hydrocortisone 14 μM, Hepes 10 mM, bFGF 1 μg/mL). RBE4 cells were stimulated for 6 h with either Aβ1-42 (3 μM) or HG (25 mM) in differentiation medium. Cells were lysed in RIPA buffer. TXNIP expression was analyzed by western blotting using a mouse anti-TXNIP monoclonal antibody (MBL). Protein loading was analyzed by western blotting of actin. (b) RBE4 cells were maintained as described in (a) and stimulated for 6 h with either Aβ1-42 (3 μM) both in the absence or presence of an anti-RAGE blocking antibody (R&D system). TXNIP expression and protein loading were analyzed by western blotting as in (a). (c) RBE4 cells were maintained as described in (a) and stimulated for 6 h with either Aβ1-42 (3 μM) or HG (25 mM) in differentiation medium. RAGE expression was analyzed by western blotting using a rabbit anti-RAGE polyclonal antibody (Santa Cruz). Protein loading was analyzed by western blotting of actin. These data are representative of 3 independent experiments.
