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Fig. 5 | Molecular Neurodegeneration

Fig. 5

From: Heparan sulfate proteoglycans mediate Aβ-induced oxidative stress and hypercontractility in cultured vascular smooth muscle cells

Fig. 5

1-40, but not Aβ1-42, induces Ca2+ influx into VSMC and this Ca2+ influx does not occur through L-type Ca2+ channels. Transformed rat cerebral VSMC were loaded with fura II (10 μM) and treated with varying concentrations of Aβ1-40 (panel a) or Aβ1-42 (panel b). In some cases, cells were treated with a scrambled control peptide (Aβ40-1; panel a) or co-treated with the NADPH oxidase inhibitor apocynin (Apo; 10 μM) and Aβ1-40 (panel c). In other experiments, cells were co-treated with an L-type Ca2+ channel antagonist (either verapamil or diltiazem; 10 μM) and Aβ1-40, or treated with Aβ1-40 in the presence or absence of the Ca2+ chelator EGTA (5 mM; panel d). Rat VSMC were also treated with aminoethoxydiphenyl borate (2APB, 10 μM), an IP3-receptor inhibitor or ryanodine (1H-Pyrrole-2-carboxylic acid, 10 μM), a Ryanodine receptor inhibitor (panel e). In some experiments, cells were pre-treated with active or heat-inactivated heparinase I (HpnI; 5 Sigma U/mL), washed, loaded with fura II, and treated with Aβ1−40 (panel f). Fluorescence was measured over ~10 minutes. Results are representative of 3 independent experiments performed in triplicate. *p < 0.05 vs. vehicle-treated control

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