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Inhibition of inducible nitric oxide synthesis by oxidized lipoprotein(a) in a murine macrophage cell line
Author(s) -
Moeslinger Thomas,
Friedl Roswitha,
Volf Ivo,
Brunner Monika,
Koller Elisabeth,
Spieckermann Paul Gerhard
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01825-1
Subject(s) - nitric oxide , lipopolysaccharide , nitric oxide synthase , chemistry , microbiology and biotechnology , macrophage , lipoprotein(a) , cell culture , lipoprotein , biochemistry , interferon gamma , biology , endocrinology , in vitro , cholesterol , genetics , organic chemistry
Increased plasma levels of human lipoprotein(a) (Lp(a)) are highly correlated with the development of atherosclerotic lesions. During our study, we investigated the effects of native and hypochlorite oxidized lipoprotein(a) (ox‐Lp(a)) on nitric oxide production by the inducible nitric oxide synthase (iNOS) in lipopolysaccharide/interferon stimulated mouse macrophages (J774A.1). Ox‐Lp(a) (0–2 μg/ml) induces a dose dependent inhibition of inducible nitric oxide synthesis. iNOS protein expression showed a dose dependent reduction as revealed by immunoblotting when cells were incubated with increasing amounts of ox‐Lp(a). Ox‐Lp(a) decreases iNOS mRNA synthesis as shown by reverse transcription‐polymerase chain reaction. Ox‐Lp(a) induced iNOS inhibition might contribute to the development of atherosclerotic lesions by reducing the anti‐atherogenic effects of nitric oxide.