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Synergistic effect of hydrogen sulfide and endotoxin on caveolin‐1 expression in liver sinusoidal endothelial cells
Author(s) -
Larion Sebastian,
Culberson Cathy,
Norris Eric,
Clemens Mark G
Publication year - 2010
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.24.1_supplement.1000.6
Subject(s) - lipopolysaccharide , chemistry , inflammation , hydrogen sulfide , nitric oxide , caveolin 1 , propidium iodide , endocrinology , medicine , biochemistry , biology , apoptosis , programmed cell death , organic chemistry , sulfur
Hydrogen sulfide (H 2 S) has been recently shown to be an important gaseous mediator during inflammation. Although H 2 S has been shown to have acute effects on blood flow in some tissues, its effects on expression of vasoregulatory proteins is not known. Since caveolin‐1(cav‐1) is an important regulator of endothelial nitric oxide synthase activity during endotoxemia, we hypothesized that H 2 S may contribute to altered vasoregulation during inflammation by modulating the effects of lipopolysaccharide (LPS) on cav‐1 expression. To test this, isolated primary rat liver sinusoidal endothelial cells (rLSECs) were treated with and without lipopolysaccharide (LPS, 100ng/ml) with increasing dosages of H 2 S (1, 50, 500 μM). H 2 S at these doses did not affect cell viability as determined by propidium iodide staining. In the absence of LPS, H 2 S treatment had no significant effect on cav‐1 expression. In contrast, LPS alone induced cav‐1 and this was potentiated by H 2 S treatment (up to approximately a 2 fold increase over LPS alone) which was significant with 50 μM H 2 S. These results suggest H 2 S has a synergistic effect on the LPS‐mediated induction of cav‐1 in rLSEC. This response may contribute to the overall effect of gaseous mediators on dysregulated liver microcirculation during inflammation. Supported by DK38201‐21.