PMID- 9888867 OWN - NLM STAT- MEDLINE DCOM- 19990420 LR - 20190831 IS - 1079-5642 (Print) IS - 1079-5642 (Linking) VI - 19 IP - 1 DP - 1999 Jan TI - Dietary omega-3, omega-6, and omega-9 unsaturated fatty acids and growth factor and cytokine gene expression in unstimulated and stimulated monocytes. A randomized volunteer study. PG - 59-66 AB - Dietary omega-3 fatty acids retard coronary atherosclerosis. Previously, we demonstrated that dietary omega-3 fatty acids reduce platelet-derived growth factor (PDGF)-A and PDGF-B mRNA levels in unstimulated, human mononuclear cells (MNCs). In a randomized, investigator-blinded intervention trial, we have now compared the effect of ingestion of 7 g/d omega-3, omega-6, or omega-9 fatty acids for 4 weeks versus no dietary intervention on PDGF-A, PDGF-B, heparin-bound epidermal growth factor (HB-EGF), monocyte chemoattractant protein-1 (MCP-1), and interleukin-10 gene expression in unstimulated MNCs and in monocytes that were adherence-activated ex vivo in a total of 28 volunteers. In unstimulated MNCs, mRNA steady-state levels of PDGF-A, PDGF-B, and MCP-1 were reduced by 25+/-10%, 31+/-13%, and 40+/-14%, respectively, after omega-3 fatty acid ingestion, as assessed by quantitative polymerase chain reaction (all P<0.05). In monocytes that were adherence-activated ex vivo for 4 and 20 hours, mRNA steady-state levels of PDGF-A, PDGF-B, and MCP-1 were reduced by 25+/-13%, 20+/-15%, and 30+/-8%, respectively (all P<0.05). Interleukin-10 and HB-EGF mRNA steady-state levels were not influenced by omega-3 fatty acid ingestion. Expression of all respective mRNAs in control volunteers or in those ingesting omega-6 or omega-9 fatty acids were not altered. We conclude that human gene expression for PDGF-A, PDGF-B, and MCP-1, factors thought relevant to atherosclerosis, is constitutive, is constant, and can be reduced only by dietary omega-3 fatty acids in unstimulated and adherence-activated monocytes. FAU - Baumann, K H AU - Baumann KH AD - Medizinische Klinik, Klinikum Innenstadt, University of Munich, Munich, Germany. FAU - Hessel, F AU - Hessel F FAU - Larass, I AU - Larass I FAU - Muller, T AU - Muller T FAU - Angerer, P AU - Angerer P FAU - Kiefl, R AU - Kiefl R FAU - von Schacky, C AU - von Schacky C LA - eng PT - Clinical Trial PT - Journal Article PT - Randomized Controlled Trial PT - Research Support, Non-U.S. Gov't PL - United States TA - Arterioscler Thromb Vasc Biol JT - Arteriosclerosis, thrombosis, and vascular biology JID - 9505803 RN - 0 (Chemokine CCL2) RN - 0 (Cytokines) RN - 0 (Dietary Fats, Unsaturated) RN - 0 (Fatty Acids, Omega-3) RN - 0 (Fatty Acids, Omega-6) RN - 0 (Fatty Acids, Unsaturated) RN - 0 (Growth Substances) RN - 0 (HBEGF protein, human) RN - 0 (Heparin-binding EGF-like Growth Factor) RN - 0 (Intercellular Signaling Peptides and Proteins) RN - 0 (Platelet-Derived Growth Factor) RN - 0 (Proto-Oncogene Proteins) RN - 0 (Proto-Oncogene Proteins c-sis) RN - 0 (RNA, Messenger) RN - 0 (platelet-derived growth factor A) RN - 130068-27-8 (Interleukin-10) RN - 62229-50-9 (Epidermal Growth Factor) SB - IM MH - Adult MH - Cells, Cultured MH - Chemokine CCL2/genetics MH - Cytokines/*genetics MH - Dietary Fats, Unsaturated/administration & dosage/*pharmacology MH - Epidermal Growth Factor/genetics MH - Fatty Acids, Omega-3/administration & dosage/pharmacology MH - Fatty Acids, Omega-6 MH - Fatty Acids, Unsaturated/administration & dosage/*pharmacology MH - *Gene Expression MH - Growth Substances/*genetics MH - Heparin-binding EGF-like Growth Factor MH - Humans MH - Intercellular Signaling Peptides and Proteins MH - Interleukin-10/genetics MH - Male MH - Monocytes/*metabolism MH - Platelet-Derived Growth Factor/genetics MH - Proto-Oncogene Proteins/genetics MH - Proto-Oncogene Proteins c-sis MH - RNA, Messenger/analysis/metabolism EDAT- 1999/01/15 00:00 MHDA- 1999/01/15 00:01 CRDT- 1999/01/15 00:00 PHST- 1999/01/15 00:00 [pubmed] PHST- 1999/01/15 00:01 [medline] PHST- 1999/01/15 00:00 [entrez] AID - 10.1161/01.atv.19.1.59 [doi] PST - ppublish SO - Arterioscler Thromb Vasc Biol. 1999 Jan;19(1):59-66. doi: 10.1161/01.atv.19.1.59.