{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,11]],"date-time":"2025-11-11T12:56:32Z","timestamp":1762865792744},"reference-count":55,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["ATVB"],"published-print":{"date-parts":[[1999,9]]},"abstract":"<jats:p><jats:italic>Abstract<\/jats:italic>\u2014Monocyte migration and activation are regulated by monocyte chemoattractant protein-1 (MCP-1). Prior studies have shown MCP-1 expression is modulated by a variety of ligands that act through extracellular receptors. In the current study, we show 9-cis retinoic acid (RA), a ligand for the nuclear hormone receptor retinoid X receptor (RXR) and retinoic acid receptor (RAR), markedly induces the expression of MCP-1. In human THP-1 monocytic leukemia cells cultured with RA (0.05 to 500 nmol\/L), MCP-1 expression was induced rapidly, significantly, and dose-dependently by as much as 165-fold. MCP-1 RNA level was also increased in RA-treated cells. Expression of PPAR\u03b3, a heterodimer partner of RXR, is also markedly induced by RA in THP-1 cells. However,<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"genpept\" xlink:href=\"BRL49653\">BRL49653<\/jats:ext-link>, a PPAR\u03b3 ligand, failed to induce MCP-1 secretion either alone or to modify the expression level induced by RA. In contrast,<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"genpept\" xlink:href=\"BRL49653\">BRL49653<\/jats:ext-link>significantly increased MCP-1 (biotinylated MCP-1) binding to THP-1 cells, whereas RA had no effect. Other peroxisome proliferator activated receptor (PPAR) ligands, 15d-PGJ<jats:sub>2<\/jats:sub>and troglitazone (PPAR\u03b3), Wy14,643 (PPAR\u03b1), and PD195599 (PPAR\u03b2) inhibited the induction of MCP-1 by RA. RA\u2019s effect on MCP-1 expression in human elutriated monocytes were similar to that observed in the THP-1 cells. These studies identify RA as a nuclear signal for MCP-1 induction in undifferentiated human monocytic cells. These studies also suggest monocyte MCP-1 expression induced through RA may modulate cell migration.<\/jats:p>","DOI":"10.1161\/01.atv.19.9.2105","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T19:44:19Z","timestamp":1308339859000},"page":"2105-2111","source":"Crossref","is-referenced-by-count":26,"title":["9-cis Retinoic Acid Induces Monocyte Chemoattractant Protein-1 Secretion in Human Monocytic THP-1 Cells"],"prefix":"10.1161","volume":"19","author":[{"given":"Lingyu","family":"Zhu","sequence":"first","affiliation":[{"name":"From the Department of Vascular and Cardiac Diseases (L.Z., C.L.B., R.S.N.), Parke-Davis Pharmaceutical Research, Ann Arbor, Mich, and The Lipid Research Laboratory (M.A.), Technion Faculty of Medicine, Rambam Medical Center and the Rappaport Family Institute for Research in the Medical Sciences and Rambam Medical Center, Haifa, Israel."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Charles L.","family":"Bisgaier","sequence":"additional","affiliation":[{"name":"From the Department of Vascular and Cardiac Diseases (L.Z., C.L.B., R.S.N.), Parke-Davis Pharmaceutical Research, Ann Arbor, Mich, and The Lipid Research Laboratory (M.A.), Technion Faculty of Medicine, Rambam Medical Center and the Rappaport Family Institute for Research in the Medical Sciences and Rambam Medical Center, Haifa, Israel."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael","family":"Aviram","sequence":"additional","affiliation":[{"name":"From the Department of Vascular and Cardiac Diseases (L.Z., C.L.B., R.S.N.), Parke-Davis Pharmaceutical Research, Ann Arbor, Mich, and The Lipid Research Laboratory (M.A.), Technion Faculty of Medicine, Rambam Medical Center and the Rappaport Family Institute for Research in the Medical Sciences and Rambam Medical Center, Haifa, Israel."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roger S.","family":"Newton","sequence":"additional","affiliation":[{"name":"From the Department of Vascular and Cardiac Diseases (L.Z., C.L.B., R.S.N.), Parke-Davis Pharmaceutical Research, Ann Arbor, Mich, and The Lipid Research Laboratory (M.A.), Technion Faculty of Medicine, Rambam Medical Center and the Rappaport Family Institute for Research in the Medical Sciences and Rambam Medical Center, Haifa, Israel."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.iy.09.040191.003153"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.3.14.2687068"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.169.4.1449"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1177\/10454411950060020101"},{"key":"e_1_3_2_5_2","doi-asserted-by":"crossref","first-page":"18318","DOI":"10.1016\/S0021-9258(17)44754-5","volume":"265","year":"1990","journal-title":"J Biol Chem"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(89)92430-3"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.88.12.5252"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.15.6953"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/atv91.12.1.1731861"},{"key":"e_1_3_2_10_2","first-page":"226","volume":"71","year":"1994","journal-title":"Lab Invest"},{"key":"e_1_3_2_11_2","first-page":"9","volume":"140","year":"1992","journal-title":"Am J Pathol"},{"key":"e_1_3_2_12_2","doi-asserted-by":"crossref","first-page":"722","DOI":"10.4049\/jimmunol.149.2.722","volume":"149","year":"1992","journal-title":"J Immunol"},{"key":"e_1_3_2_13_2","doi-asserted-by":"crossref","unstructured":"Safirstein R Megyesi J Saggi SJ Price PM Poon M Rollins BJ Taubman MB. 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