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Effect of hyperketonemia and L‐cysteine on monocyte adhesion to endothelial cells
Author(s) -
Kanikarla-Marie Preeti,
Jain Sushil K.
Publication year - 2012
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.26.1_supplement.633.5
Subject(s) - monocyte , adhesion , cell adhesion , cysteine , chemistry , cell adhesion molecule , endothelial stem cell , medicine , endothelium , endocrinology , immunology , biochemistry , in vitro , enzyme , organic chemistry
Frequent episodes of hyperketonemia are associated with higher incidences of vascular disease in type 1 diabetic patients. Previous studies demonstrate that hyperketonemia increases monocyte‐endothelial cell (EC) adhesion. L‐Cysteine is a semi‐essential amino acid with a free sulfhydryl group. Type 1 diabetic patients have lower blood levels of L‐cysteine. This study has examined the hypothesis that supplementation with L‐cysteine can decrease monocyte adhesion to endothelial cells and thereby delay or prevent vascular disease in type 1 diabetes. Human THP‐1 monocytes and Human umbilical venule endothelial cells (HUVECs) were cultured with acetoacetate (0–8 mM) for 24 hours. Monocyte adhesion to HUVECs was determined by using cell tracker green dye. Results show that there was an increase in monocyte adhesion to HUVEC monolayer¡¦s treated with 6 mM aetoacetate compared with control. Monocyte adhesion was blocked by almost 12% (p=0.04) when monocytes and HUVEC¡¦s were pre‐incubated with L‐cysteine (500 ƒÝM) for 4 hours before exposure to acetoacetate. This suggests that, L‐cysteine supplementation can lower monocyte adhesion to endothelium. Whether or not L‐cysteine inhibition of monocyte adhesion to ECs is mediated by down‐regulation of LFA‐1, CD‐14 and ICAM‐1 needs to be investigated. Supported by NIH and Office of Dietary Supplements (RO1 DK 072433) and Malcolm Feist Chair in Diabetes.