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Effects of humic acid on the viability and coagulant properties of human umbilical vein endothelial cells
Author(s) -
Yang HsinLing,
Chiu HuiChong,
Lu FungJou
Publication year - 1996
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/(sici)1096-8652(199603)51:3<200::aid-ajh4>3.0.co;2-0
Subject(s) - umbilical vein , viability assay , plasminogen activator , fetal bovine serum , chemistry , fibrinolysis , microbiology and biotechnology , cytotoxic t cell , tissue plasminogen activator , human umbilical vein endothelial cell , plasminogen activator inhibitor 1 , endothelial stem cell , cytotoxicity , andrology , biochemistry , biology , cell , in vitro , medicine , endocrinology
We have previously shown that humic acid (well‐water humic acid, HA, and synthetic humic acid, SHA) enhances cell surface expression of tissue factor (TF). Here we report that incubation of human umbilical vein endothelial cells (HUVEC) for 2 hr with HA or SHA cause a rapid rise in TF mRNA levels, as shown by Northern blot analysis. To understand the cytotoxic and fibrinolytic effects of HA and SHA on cultured HUVEC, the cells were treated with varying concentrations of HA and SHA for various periods of time. Both HA and SHA (10–200 μg/ml) inhibited the viability of subconfluent HUVEC, cultured in the presence or absence of 20% FBS (Fetal Bovine serum) in the culture medium, in a dose‐dependent manner. Both HA and SHA induced surface changes in the HUVEC as revealed by scanning electron micrography (SEM). However, protocatechuic acid, the monomer of SHA, did not significantly inhibit cell growth, and showed a cytotoxic effect only at 200 μg/ml. Furthermore both HA and SHA stimulated HUVEC to produce plasminogen activator inhibitor (PAI‐1) and tissue plasminogen activator (t‐PA) in a dose and time dependent fashion; the amount of PAI‐1 produced was found to exceed that of t‐PA. The monomer of SHA did not have this stimulatory effect. These results distinctly suggest that in addition to the inhibition of viability HA is involved in TF induction and PAI‐1 synthesis in HUVEC and these may be some of the plausible mechanisms underlying the thrombotic disorders in Blackfoot disease. © 1996 Wiley‐Liss, Inc.