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Endothelial Glycocalyx and Apoptosis in Atherosclerosis
Author(s) -
Cancel Limary,
Ebong Eno,
Tarbell John
Publication year - 2015
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.29.1_supplement.631.3
Subject(s) - glycocalyx , apoptosis , apolipoprotein e , knockout mouse , vascular permeability , endothelium , apolipoprotein b , lipoprotein , medicine , chemistry , biology , pathology , endocrinology , immunology , cholesterol , disease , biochemistry , receptor
Elevated permeability of vascular endothelium to low density lipoprotein (LDL) is characteristic of focal sites within the vasculature that are prone to the development of atherosclerosis. Previous experiments have suggested that both increased endothelial cell (EC) apoptosis and endothelial surface glycocalyx (GCX) shedding could play a role in the elevated LDL permeability of athero‐prone regions. In this work, we sought to confirm that GCX shedding and increased EC apoptosis do occur in lipid plaque filled vessel areas. Six 4‐ to 6‐week old male C57Bl/6 apolipoprotein E knockout (ApoE) mice were fed a Western diet for 10 weeks and developed raised plaques in their brachiocephalic arteries (BCA). Our results show that EC apoptosis is significantly increased throughout the vasculature of ApoE mice compared with wild type mice fed a normal diet. More importantly, we demonstrate that the number of apoptotic ECs per unit length is 3 times higher in the plaque region of the BCA of ApoE mice than in the non‐plaque region of the same vessel. We also show that GCX coverage and thickness are significantly reduced over the plaque region compared to the non‐plaque region, where values are not different from those found in the wild type mice. Our results suggest that both increased EC apoptosis and GCX are involved in the development of atherosclerotic plaques. Research supported by NIH HL094889.