JCI - Hyperhomocysteinemia enhances vascular inflammation and accelerates atherosclerosis in a murine model

Hyperhomocysteinemia enhances vascular inflammation and accelerates atherosclerosis in a murine model

Marion A. Hofmann, Evanthia Lalla, Yan Lu, Michelle Ryu Gleason, Bonnie M. Wolf, Nozomu Tanji, Luis J. Ferran Jr., Brigitte Kohl, Vijay Rao, Walter Kisiel, David M. Stern, Ann Marie Schmidt

Published in Volume 107, Issue 6

J Clin Invest. 2001; 107(6):675–683 doi:10.1172/JCI10588

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Figure 2

HHcy enhances activation of NF-κB as seen using EMSA. (a) HUVECs were exposed to BSA, L-HC, or L-cysteine (100 μM) for 8 hours. Nuclear extracts were prepared and subjected to EMSA. ^AP < 0.05 vs. lanes 1 and 3. In lane 4, a 100-fold molar excess of unlabeled NF-κB was added to indicate specificity for NF-κB. (b) After 8 weeks of diet, apoE-null mice were sacrificed and nuclear extracts prepared from kidney (lanes 1–3) or aorta (lanes 4–6) for EMSA. ^BP < 0.01 vs. lanes 1 and 3 and 4 and 6, respectively. EMSA was performed on n = 7 mice/diet; representative experiments are shown. Densitometric analysis was performed; pixels obtained from analysis of EMSA on BSA-treated samples or tissue samples from animals receiving diet A were arbitrarily assigned a relative value of 1.