Fig. 3
Pharmacological knockdown of other glycosaminoglycan (GAG) family members does not affect Aβ1-40-mediated ROS production in VSMC. Primary human cerebral VSMC were pre-treated with chondroitinase B (10-1 IU/mL; selectively degrades dermatin sulfate; panel a), chondroitinase AC (10-1 IU/mL; selectively degrades chondroitin sulfate; panel a), or varying concentrations of the sulfation inhibitor sodium chlorate (5-50 mM; panel b) for 2 h, washed, loaded with Mitotracker Red CM-H2XRos (MTR; 5 μM), and treated with Aβ1-40. In some cases, cells were pre-treated with heat-inactivated (HI) enzyme (at the same concentration of active enzyme) and washed prior to MTR loading and Aβ treatment. Fluorescence was measured after 30 minutes. Results are representative of 3 independent experiments performed in triplicate. *p < 0.05 vs. vehicle-treated control. #p < 0.05 vs. comparison group