Adiponectin reduces atherosclerosis in apolipoprotein E-deficient mice
Dysregulation of adipocyte-derived bioactive molecules plays an important role in the development of atherosclerosis. We previously reported that adiponectin, an adipocyte-specific plasma protein, accumulated in the injured artery from the plasma and suppressed endothelial inflammatory response and...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2002-11, Vol.106 (22), p.2767-2770 |
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| creator | OKAMOTO, Yoshihisa KIHARA, Shinji TERASAKA, Naoki INABA, Toshimori FUNAHASHI, Tohru MATSUZAWA, Yuji OUCHI, Noriyuki NISHIDA, Makoto ARITA, Yukio KUMADA, Masahiro OHASHI, Koji SAKAI, Naohiko SHIMOMURA, Iichiro KOBAYASHI, Hideki |
| description | Dysregulation of adipocyte-derived bioactive molecules plays an important role in the development of atherosclerosis. We previously reported that adiponectin, an adipocyte-specific plasma protein, accumulated in the injured artery from the plasma and suppressed endothelial inflammatory response and vascular smooth muscle cell proliferation, as well as macrophage-to-foam cell transformation in vitro. The current study investigated whether the increased plasma adiponectin could actually reduce atherosclerosis in vivo.
Apolipoprotein E-deficient mice were treated with recombinant adenovirus expressing human adiponectin (Ad-APN) or beta-galactosidase (Ad-betagal). The plasma adiponectin levels in Ad-APN-treated mice increased 48 times as much as those in Ad-betagal treated mice. On the 14th day after injection, the lesion formation in aortic sinus was inhibited in Ad-APN-treated mice by 30% compared with Ad-betagal-treated mice (P |
| doi_str_mv | 10.1161/01.cir.0000042707.50032.19 |
| format | Article |
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Apolipoprotein E-deficient mice were treated with recombinant adenovirus expressing human adiponectin (Ad-APN) or beta-galactosidase (Ad-betagal). The plasma adiponectin levels in Ad-APN-treated mice increased 48 times as much as those in Ad-betagal treated mice. On the 14th day after injection, the lesion formation in aortic sinus was inhibited in Ad-APN-treated mice by 30% compared with Ad-betagal-treated mice (P<0.05). In the lesions of Ad-APN-treated mice, the lipid droplets became smaller compared with Ad-betagal-treated mice (P<0.01). Immunohistochemical analyses demonstrated that the adenovirus-mediated adiponectin migrate to foam cells in the fatty streak lesions. The real-time quantitative polymerase chain reaction revealed that Ad-APN treatment significantly suppressed the mRNA levels of vascular cell adhesion molecule-1 by 29% and class A scavenger receptor by 34%, and tended to reduce levels of tumor necrosis factor-alpha without affecting those of CD36 in the aortic tissue.
These findings documented for the first time that elevated plasma adiponectin suppresses the development of atherosclerosis in vivo.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.cir.0000042707.50032.19</identifier><identifier>PMID: 12451000</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Adiponectin ; Animals ; Apolipoproteins E - blood ; Apolipoproteins E - deficiency ; Apolipoproteins E - genetics ; Arteriosclerosis - genetics ; Arteriosclerosis - pathology ; Arteriosclerosis - prevention & control ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; CD36 Antigens - genetics ; CD36 Antigens - metabolism ; Disease Models, Animal ; Disease Progression ; Foam Cells - metabolism ; Foam Cells - pathology ; Genetic Therapy ; Genetic Vectors - administration & dosage ; Genetic Vectors - genetics ; Immunohistochemistry ; Intercellular Signaling Peptides and Proteins ; Macrophages - pathology ; Male ; Medical sciences ; Membrane Proteins ; Mice ; Mice, Knockout ; Muscle, Smooth, Vascular - pathology ; Proteins - genetics ; Proteins - metabolism ; Proteins - pharmacology ; Receptors, Immunologic - genetics ; Receptors, Immunologic - metabolism ; Receptors, Lipoprotein ; Receptors, Scavenger ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - analysis ; RNA, Messenger - metabolism ; Scavenger Receptors, Class A ; Scavenger Receptors, Class B ; Sinus of Valsalva - drug effects ; Sinus of Valsalva - pathology ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Vascular Cell Adhesion Molecule-1 - genetics ; Vascular Cell Adhesion Molecule-1 - metabolism</subject><ispartof>Circulation (New York, N.Y.), 2002-11, Vol.106 (22), p.2767-2770</ispartof><rights>2003 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Nov 26, 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c538t-adfd3f96b13df9a94482ac4ee37751ef68b67a5f4a0d5e989b6ab16d017cbb463</citedby><cites>FETCH-LOGICAL-c538t-adfd3f96b13df9a94482ac4ee37751ef68b67a5f4a0d5e989b6ab16d017cbb463</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14921645$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12451000$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>OKAMOTO, Yoshihisa</creatorcontrib><creatorcontrib>KIHARA, Shinji</creatorcontrib><creatorcontrib>TERASAKA, Naoki</creatorcontrib><creatorcontrib>INABA, Toshimori</creatorcontrib><creatorcontrib>FUNAHASHI, Tohru</creatorcontrib><creatorcontrib>MATSUZAWA, Yuji</creatorcontrib><creatorcontrib>OUCHI, Noriyuki</creatorcontrib><creatorcontrib>NISHIDA, Makoto</creatorcontrib><creatorcontrib>ARITA, Yukio</creatorcontrib><creatorcontrib>KUMADA, Masahiro</creatorcontrib><creatorcontrib>OHASHI, Koji</creatorcontrib><creatorcontrib>SAKAI, Naohiko</creatorcontrib><creatorcontrib>SHIMOMURA, Iichiro</creatorcontrib><creatorcontrib>KOBAYASHI, Hideki</creatorcontrib><title>Adiponectin reduces atherosclerosis in apolipoprotein E-deficient mice</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Dysregulation of adipocyte-derived bioactive molecules plays an important role in the development of atherosclerosis. We previously reported that adiponectin, an adipocyte-specific plasma protein, accumulated in the injured artery from the plasma and suppressed endothelial inflammatory response and vascular smooth muscle cell proliferation, as well as macrophage-to-foam cell transformation in vitro. The current study investigated whether the increased plasma adiponectin could actually reduce atherosclerosis in vivo.
Apolipoprotein E-deficient mice were treated with recombinant adenovirus expressing human adiponectin (Ad-APN) or beta-galactosidase (Ad-betagal). The plasma adiponectin levels in Ad-APN-treated mice increased 48 times as much as those in Ad-betagal treated mice. On the 14th day after injection, the lesion formation in aortic sinus was inhibited in Ad-APN-treated mice by 30% compared with Ad-betagal-treated mice (P<0.05). In the lesions of Ad-APN-treated mice, the lipid droplets became smaller compared with Ad-betagal-treated mice (P<0.01). Immunohistochemical analyses demonstrated that the adenovirus-mediated adiponectin migrate to foam cells in the fatty streak lesions. The real-time quantitative polymerase chain reaction revealed that Ad-APN treatment significantly suppressed the mRNA levels of vascular cell adhesion molecule-1 by 29% and class A scavenger receptor by 34%, and tended to reduce levels of tumor necrosis factor-alpha without affecting those of CD36 in the aortic tissue.
These findings documented for the first time that elevated plasma adiponectin suppresses the development of atherosclerosis in vivo.</description><subject>Adiponectin</subject><subject>Animals</subject><subject>Apolipoproteins E - blood</subject><subject>Apolipoproteins E - deficiency</subject><subject>Apolipoproteins E - genetics</subject><subject>Arteriosclerosis - genetics</subject><subject>Arteriosclerosis - pathology</subject><subject>Arteriosclerosis - prevention & control</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>CD36 Antigens - genetics</subject><subject>CD36 Antigens - metabolism</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Foam Cells - metabolism</subject><subject>Foam Cells - pathology</subject><subject>Genetic Therapy</subject><subject>Genetic Vectors - administration & dosage</subject><subject>Genetic Vectors - genetics</subject><subject>Immunohistochemistry</subject><subject>Intercellular Signaling Peptides and Proteins</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Proteins</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>Proteins - pharmacology</subject><subject>Receptors, Immunologic - genetics</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Receptors, Lipoprotein</subject><subject>Receptors, Scavenger</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - analysis</subject><subject>RNA, Messenger - metabolism</subject><subject>Scavenger Receptors, Class A</subject><subject>Scavenger Receptors, Class B</subject><subject>Sinus of Valsalva - drug effects</subject><subject>Sinus of Valsalva - pathology</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Vascular Cell Adhesion Molecule-1 - genetics</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkd9LHDEQx0Ox6NX6L8gh6NtuM_m58U0ObQWhUNrnkE0mNLK3eya7D_735vTgwDxM-DKfmUy-Q8gV0BZAwQ8KrU-5pfsjmKa6lZRy1oL5QlYgmWiE5OaErGreNJozdka-lfJcpeJanpIzYEJClSvycBfSbhrRz2lcZwyLx7J283_MU_HDPqayrim3m4YK7vI0Y5X3TcCYfMJxXm-Tx-_ka3RDwYvDfU7-Pdz_3fxqnn7_fNzcPTVe8m5uXIiBR6N64CEaZ4TomPMCkWstAaPqeqWdjMLRINF0pleuBxUoaN_3QvFzcvPRtw7ysmCZ7TYVj8PgRpyWYnW1w0gFFbz6BD5PSx7rbJYB09wo3lXo9gPy9Z8lY7S7nLYuv1qgdm-1pWA3j3_s0Wr7brUFU4svDy8s_RbDsfTgbQWuD4Ar3g0xu9GncuSEYaDqpt4AF62Hrw</recordid><startdate>20021126</startdate><enddate>20021126</enddate><creator>OKAMOTO, Yoshihisa</creator><creator>KIHARA, Shinji</creator><creator>TERASAKA, Naoki</creator><creator>INABA, Toshimori</creator><creator>FUNAHASHI, Tohru</creator><creator>MATSUZAWA, Yuji</creator><creator>OUCHI, Noriyuki</creator><creator>NISHIDA, Makoto</creator><creator>ARITA, Yukio</creator><creator>KUMADA, Masahiro</creator><creator>OHASHI, Koji</creator><creator>SAKAI, Naohiko</creator><creator>SHIMOMURA, Iichiro</creator><creator>KOBAYASHI, Hideki</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20021126</creationdate><title>Adiponectin reduces atherosclerosis in apolipoprotein E-deficient mice</title><author>OKAMOTO, Yoshihisa ; KIHARA, Shinji ; TERASAKA, Naoki ; INABA, Toshimori ; FUNAHASHI, Tohru ; MATSUZAWA, Yuji ; OUCHI, Noriyuki ; NISHIDA, Makoto ; ARITA, Yukio ; KUMADA, Masahiro ; OHASHI, Koji ; SAKAI, Naohiko ; SHIMOMURA, Iichiro ; KOBAYASHI, Hideki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c538t-adfd3f96b13df9a94482ac4ee37751ef68b67a5f4a0d5e989b6ab16d017cbb463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adiponectin</topic><topic>Animals</topic><topic>Apolipoproteins E - blood</topic><topic>Apolipoproteins E - deficiency</topic><topic>Apolipoproteins E - genetics</topic><topic>Arteriosclerosis - genetics</topic><topic>Arteriosclerosis - pathology</topic><topic>Arteriosclerosis - prevention & control</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>CD36 Antigens - genetics</topic><topic>CD36 Antigens - metabolism</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Foam Cells - metabolism</topic><topic>Foam Cells - pathology</topic><topic>Genetic Therapy</topic><topic>Genetic Vectors - administration & dosage</topic><topic>Genetic Vectors - genetics</topic><topic>Immunohistochemistry</topic><topic>Intercellular Signaling Peptides and Proteins</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Proteins</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>Proteins - pharmacology</topic><topic>Receptors, Immunologic - genetics</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Receptors, Lipoprotein</topic><topic>Receptors, Scavenger</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - analysis</topic><topic>RNA, Messenger - metabolism</topic><topic>Scavenger Receptors, Class A</topic><topic>Scavenger Receptors, Class B</topic><topic>Sinus of Valsalva - drug effects</topic><topic>Sinus of Valsalva - pathology</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Vascular Cell Adhesion Molecule-1 - genetics</topic><topic>Vascular Cell Adhesion Molecule-1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>OKAMOTO, Yoshihisa</creatorcontrib><creatorcontrib>KIHARA, Shinji</creatorcontrib><creatorcontrib>TERASAKA, Naoki</creatorcontrib><creatorcontrib>INABA, Toshimori</creatorcontrib><creatorcontrib>FUNAHASHI, Tohru</creatorcontrib><creatorcontrib>MATSUZAWA, Yuji</creatorcontrib><creatorcontrib>OUCHI, Noriyuki</creatorcontrib><creatorcontrib>NISHIDA, Makoto</creatorcontrib><creatorcontrib>ARITA, Yukio</creatorcontrib><creatorcontrib>KUMADA, Masahiro</creatorcontrib><creatorcontrib>OHASHI, Koji</creatorcontrib><creatorcontrib>SAKAI, Naohiko</creatorcontrib><creatorcontrib>SHIMOMURA, Iichiro</creatorcontrib><creatorcontrib>KOBAYASHI, Hideki</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>OKAMOTO, Yoshihisa</au><au>KIHARA, Shinji</au><au>TERASAKA, Naoki</au><au>INABA, Toshimori</au><au>FUNAHASHI, Tohru</au><au>MATSUZAWA, Yuji</au><au>OUCHI, Noriyuki</au><au>NISHIDA, Makoto</au><au>ARITA, Yukio</au><au>KUMADA, Masahiro</au><au>OHASHI, Koji</au><au>SAKAI, Naohiko</au><au>SHIMOMURA, Iichiro</au><au>KOBAYASHI, Hideki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adiponectin reduces atherosclerosis in apolipoprotein E-deficient mice</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2002-11-26</date><risdate>2002</risdate><volume>106</volume><issue>22</issue><spage>2767</spage><epage>2770</epage><pages>2767-2770</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Dysregulation of adipocyte-derived bioactive molecules plays an important role in the development of atherosclerosis. We previously reported that adiponectin, an adipocyte-specific plasma protein, accumulated in the injured artery from the plasma and suppressed endothelial inflammatory response and vascular smooth muscle cell proliferation, as well as macrophage-to-foam cell transformation in vitro. The current study investigated whether the increased plasma adiponectin could actually reduce atherosclerosis in vivo.
Apolipoprotein E-deficient mice were treated with recombinant adenovirus expressing human adiponectin (Ad-APN) or beta-galactosidase (Ad-betagal). The plasma adiponectin levels in Ad-APN-treated mice increased 48 times as much as those in Ad-betagal treated mice. On the 14th day after injection, the lesion formation in aortic sinus was inhibited in Ad-APN-treated mice by 30% compared with Ad-betagal-treated mice (P<0.05). In the lesions of Ad-APN-treated mice, the lipid droplets became smaller compared with Ad-betagal-treated mice (P<0.01). Immunohistochemical analyses demonstrated that the adenovirus-mediated adiponectin migrate to foam cells in the fatty streak lesions. The real-time quantitative polymerase chain reaction revealed that Ad-APN treatment significantly suppressed the mRNA levels of vascular cell adhesion molecule-1 by 29% and class A scavenger receptor by 34%, and tended to reduce levels of tumor necrosis factor-alpha without affecting those of CD36 in the aortic tissue.
These findings documented for the first time that elevated plasma adiponectin suppresses the development of atherosclerosis in vivo.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>12451000</pmid><doi>10.1161/01.cir.0000042707.50032.19</doi><tpages>4</tpages></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 2002-11, Vol.106 (22), p.2767-2770 |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Adiponectin Animals Apolipoproteins E - blood Apolipoproteins E - deficiency Apolipoproteins E - genetics Arteriosclerosis - genetics Arteriosclerosis - pathology Arteriosclerosis - prevention & control Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system CD36 Antigens - genetics CD36 Antigens - metabolism Disease Models, Animal Disease Progression Foam Cells - metabolism Foam Cells - pathology Genetic Therapy Genetic Vectors - administration & dosage Genetic Vectors - genetics Immunohistochemistry Intercellular Signaling Peptides and Proteins Macrophages - pathology Male Medical sciences Membrane Proteins Mice Mice, Knockout Muscle, Smooth, Vascular - pathology Proteins - genetics Proteins - metabolism Proteins - pharmacology Receptors, Immunologic - genetics Receptors, Immunologic - metabolism Receptors, Lipoprotein Receptors, Scavenger Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - analysis RNA, Messenger - metabolism Scavenger Receptors, Class A Scavenger Receptors, Class B Sinus of Valsalva - drug effects Sinus of Valsalva - pathology Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Vascular Cell Adhesion Molecule-1 - genetics Vascular Cell Adhesion Molecule-1 - metabolism |
| title | Adiponectin reduces atherosclerosis in apolipoprotein E-deficient mice |
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