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Endothelial apoptosis and glycocalyx morphology in plaque and non‐plaque areas of the mouse atherosclerotic brachiocephalic artery
Author(s) -
Cancel Limary Melissa,
Ebong Eno E,
Tarbell John M
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.869.4
Subject(s) - glycocalyx , apoptosis , vascular permeability , fibrous cap , pathology , in vitro , chemistry , apolipoprotein b , biology , microbiology and biotechnology , medicine , biochemistry , cholesterol
The vascular endothelial cell (EC) layer defends against atherosclerosis. Animal experiments have suggested that both increased EC apoptosis and shedding of the EC surface glycocalyx layer (EGL) play a role in elevated low density lipoprotein (LDL) permeability, a characteristic feature of atherosclerotic‐prone vascular regions. Recently, we confirmed in vitro that LDL permeability correlates strongly with measured apoptosis rates. We have also observed that a compound that enhances the EGL leads to dramatic reductions in LDL permeability in vitro . In the present study, we further elucidate the role of EC apoptosis and the EGL in atherosclerotic plaque formation. Atherosclerotic brachiocephalic (BCA) arteries were dissected from high fat fed Apolipoprotein‐E‐null mice. Fluorescent stained 6‐μm thick BCA cryosections revealed elevated EC apoptosis and degraded EGL on the plaque‐covered vascular wall, compared to non‐plaque areas. This is the first study to visualize the EGL morphology overlying an atherosclerotic lesion, and to compare EGL degradation and EC apoptosis in plaque development. Research support: NIH HL094889 .