Leukocyte ABCA1 controls susceptibility to atherosclerosis and macrophage recruitment into tissues

DOI Web Site 被引用文献6件
  • Miranda Van Eck
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121
  • I. Sophie T. Bos
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121
  • Wolfgang E. Kaminski
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121
  • Evelyn Orsó
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121
  • Gregor Rothe
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121
  • Jaap Twisk
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121
  • Alfred Böttcher
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121
  • Edwin S. Van Amersfoort
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121
  • Trudy A. Christiansen-Weber
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121
  • Wai-Ping Fung-Leung
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121
  • Theo J. C. Van Berkel
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121
  • Gerd Schmitz
    Division of Biopharmaceutics, Leiden/Amsterdam Center for Drug Research, Sylvius Laboratories, Leiden University, P.O. Box 9503, 2300 RA Leiden, The Netherlands; Institute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, D-93042 Regensburg, Germany; and R. W. Johnson Pharmaceutical Research Institute, San Diego, CA 92121

書誌事項

公開日
2002-04-23
DOI
  • 10.1073/pnas.092327399
公開者
Proceedings of the National Academy of Sciences

この論文をさがす

説明

<jats:p> The ATP-binding cassette transporter 1 (ABCA1) has recently been identified as a key regulator of high-density lipoprotein (HDL) metabolism, which is defective in familial HDL-deficiency syndromes such as Tangier disease. ABCA1 functions as a facilitator of cellular cholesterol and phospholipid efflux, and its expression is induced during cholesterol uptake in macrophages. To assess the role of macrophage ABCA1 in atherosclerosis, we generated low-density lipoprotein (LDL) receptor knockout (LDLr <jats:sup>−/−</jats:sup> ) mice that are selectively deficient in leukocyte ABCA1 (ABCA1 <jats:sup>−/−</jats:sup> ) by using bone marrow transfer (ABCA1 <jats:sup>−/−</jats:sup> → LDLr <jats:sup>−/−</jats:sup> ). Here we demonstrate that ABCA1 <jats:sup>−/−</jats:sup> → LDLr <jats:sup>−/−</jats:sup> chimeras develop significantly larger and more advanced atherosclerotic lesions compared with chimeric LDLr <jats:sup>−/−</jats:sup> mice with functional ABCA1 in hematopoietic cells. Targeted disruption of leukocyte ABCA1 function did not affect plasma HDL cholesterol levels. The amount of macrophages in liver and spleen and peripheral blood leukocyte counts is increased in the ABCA1 <jats:sup>−/−</jats:sup> → LDLr <jats:sup>−/−</jats:sup> chimeras. Our results provide evidence that leukocyte ABCA1 plays a critical role in the protection against atherosclerosis, and we identify ABCA1 as a leukocyte factor that controls the recruitment of inflammatory cells. </jats:p>

収録刊行物

被引用文献 (6)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ