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Effect of vitamin‐D on ROS, ICAM‐1 and monocyte adhesion in human umbilical vein endothelial cells (HUVECs) treated with high glucose and acetoacetate
Author(s) -
KanikarlaMarie Preeti,
Jain Sushil K.
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.1078.15
Subject(s) - umbilical vein , monocyte , icam 1 , nadph oxidase , endothelial dysfunction , medicine , endocrinology , chemistry , endothelium , adhesion , reactive oxygen species , oxidative stress , cell adhesion molecule , biochemistry , immunology , in vitro , organic chemistry
Monocyte adhesion to the endothelium plays a central role in the progression of endothelial dysfunction and cardiovascular disease (CVD). Epidemiological studies report a relationship between vitamin‐D (VD) deficiency and increased risk of CVD in diabetic patients. This study examines whether or not VD supplementation is beneficial in preventing endothelial dysfunction in diabetes. HUVECs were treated with 1, 25‐(OH)2‐D3 (0–50nM) for 24h, and later exposed to the ketone body acetoacetate (AA; 0, 2, 4, 8mM) or high glucose (HG, 25mM) for 24h. There was an increase in ROS, ICAM‐1 expression, and monocyte adhesion in HUVECs treated with AA or HG. VD (50nM) supplementation lowered ROS (41%, p<0.05), ICAM‐1 (73%, p=0.05) and p‐NFêB (50%, p<0.05) expression, and IL‐8 (16%, p=0.05) and MCP‐1 (41.2%, p<0.001) secretion in HUVECs treated with AA. VD significantly inhibited (37.5%, p=0.05) monocyte adhesion to HUVECs exposed to AA. VD had a similar beneficial effect on HUVECs treated with HG. Apocyanin (NADPH oxidase inhibitor), reduced ROS in HG or AA treated HUVECs. The role of VD in inhibiting NADPH oxidases and ROS is under investigation. This study provides the biochemical mechanism through which VD supplementation can lower ROS, ICAM‐1 expression, monocyte adhesion to the endothelium, and thereby the risk of CVD in diabetes. Grant Funding Source : NIDDK and Office of Dietary Supplements