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Linoleic Acid Regulates the Expression of Oxidized Low Density Lipoprotein Receptor (OLR1) in 3T3‐L1 Adipocytes via ERK and JNK Pathways
Author(s) -
Ajuwon Kolapo Matthew,
Franklin Dru M,
Banz William J,
Winters Todd A
Publication year - 2007
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.21.5.a455-c
Subject(s) - cd36 , linoleic acid , chemistry , mapk/erk pathway , medicine , endocrinology , kinase , bisindolylmaleimide , protein kinase c , receptor , biochemistry , fatty acid
Dietary fatty acids modulate the risks for heart diseases. Our objective was to investigate the role of 2 common dietary fatty acids, palmitic and linoleic acids, in the regulation of the two major receptors for oxidized LDL, CD36 and OLR1, in fully differentiated 3T3‐L1 adipocytes. Differentiated adipocytes were treated with BSA‐bound fatty acids at 250 and 500μM concentrations for 6 and 24 hours. Expression of CD36 and OLR1 was determined by western blotting and real‐time PCR. OLR1 but not CD36 was robustly induced by linoleic acid (P<0.05) at 6 hours and sustained for 24 hours. Palmitate also induced OLR1, albeit to a lesser degree and only after 24 hours of exposure. We used specific MAP kinase inhibitors (U0126 and SP600125 for ERK and c‐JNK respectively), PKC inhibitor (Bisindolylmaleimide) and the NF‐kappa B inhibitor (Bay 11‐7082), to investigate the involvement of these pathways in the induction of OLR1 by linoleic acid. Inhibition of ERK and c‐JNK suppressed linoleic acid induction of OLR1 (P<0.05). However, inhibition of PKC and NF‐kappa B had no significant effect. Therefore, ERK and JNK pathways are important regulators of OLR1 expression in adipocytes.