Repopulation of Apolipoprotein E Knockout Mice With CCR2-Deficient Bone Marrow Progenitor Cells Does Not Inhibit Ongoing Atherosclerotic Lesion Development
OBJECTIVE—Using bone marrow transplantation, we have previously demonstrated the critical role that hematopoietic CCR2 plays in early atherogenesis. Reconstitution of irradiated apolipoprotein (apo) E3–Leiden mice with CCR2-deficient bone marrow progenitor cells resulted in 86% reduction on overall...
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| creator | Guo, Jian de Waard, Vivian Van Eck, Miranda Hildebrand, Reeni B van Wanrooij, Eva J.A Kuiper, Johan Maeda, Nobuyo Benson, G Martin Groot, Pieter H.E Van Berkel, Theo J.C |
| description | OBJECTIVE—Using bone marrow transplantation, we have previously demonstrated the critical role that hematopoietic CCR2 plays in early atherogenesis. Reconstitution of irradiated apolipoprotein (apo) E3–Leiden mice with CCR2-deficient bone marrow progenitor cells resulted in 86% reduction on overall atherosclerotic lesion development. However, no data on CCR2 in the cause of established atherosclerosis have been reported so far.
METHODS AND RESULTS—To study the role of CCR2 in established atherosclerotic lesions, bone marrow progenitor cells harvested from apoE and apoE/CCR2 mice were transplanted into lethally irradiated 16-week-old apoE mice with established atherosclerotic lesions. No significant differences were found in serum total cholesterol and triglycerides levels at different time points after transplantation. At age 16 weeks, lesion size in control apoE mice was 3.28±1.06×10 μm. At 9 weeks after transplantation, apoE→ apoE and apoE/CCR2→ apoE mice had developed significantly larger atherosclerotic lesions (4.49±0.92×10 μm, P |
| doi_str_mv | 10.1161/01.ATV.0000163181.40896.42 |
| format | Article |
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METHODS AND RESULTS—To study the role of CCR2 in established atherosclerotic lesions, bone marrow progenitor cells harvested from apoE and apoE/CCR2 mice were transplanted into lethally irradiated 16-week-old apoE mice with established atherosclerotic lesions. No significant differences were found in serum total cholesterol and triglycerides levels at different time points after transplantation. At age 16 weeks, lesion size in control apoE mice was 3.28±1.06×10 μm. At 9 weeks after transplantation, apoE→ apoE and apoE/CCR2→ apoE mice had developed significantly larger atherosclerotic lesions (4.49±0.92×10 μm, P<0.02 and 4.15±0.62×10 μm, P<0.04 compared with controls, respectively). However, no significant effect of disruption of hematopoietic CCR2 was observed on the progression of lesions. Furthermore, the macrophage positive area (78±4% versus 72±9%) and collagen content (11±6% versus 15±3%) of the lesions were similar as well.
CONCLUSION—In contrast to the critical role of CCR2 in the initiation of atherogenesis, bone marrow progenitor cell-derived CCR2 does not influence the progression of established atherosclerotic lesions, pointing to additional mechanisms for recruitment of monocytes at later stages of lesion development.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000163181.40896.42</identifier><identifier>PMID: 15774908</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Apolipoproteins E - genetics ; Atherosclerosis (general aspects, experimental research) ; Atherosclerosis - immunology ; Atherosclerosis - pathology ; Atherosclerosis - therapy ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood vessels and receptors ; Bone Marrow Transplantation ; Cardiology. Vascular system ; Cell Movement - drug effects ; Cell Movement - immunology ; Cholesterol - blood ; Collagen - metabolism ; Disease Progression ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Female ; Fundamental and applied biological sciences. Psychology ; Hematopoietic Stem Cell Transplantation ; Lymph Nodes - cytology ; Lymph Nodes - immunology ; Macrophages, Peritoneal - pathology ; Medical sciences ; Mice ; Mice, Knockout ; Monocytes - pathology ; Peritonitis - chemically induced ; Peritonitis - immunology ; Radiation Chimera ; Receptors, CCR2 ; Receptors, Chemokine - genetics ; T-Lymphocytes - immunology ; Thioglycolates - pharmacology ; Triglycerides - blood ; Vertebrates: cardiovascular system</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2005-05, Vol.25 (5), p.1014-1019</ispartof><rights>2005 American Heart Association, Inc.</rights><rights>2005 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. May 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5623-cb484a9cc61a82d9ebaa40a29f452f05c3b283c1c1b5ee09fcd1b4fca10df18f3</citedby><cites>FETCH-LOGICAL-c5623-cb484a9cc61a82d9ebaa40a29f452f05c3b283c1c1b5ee09fcd1b4fca10df18f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16785415$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15774908$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Jian</creatorcontrib><creatorcontrib>de Waard, Vivian</creatorcontrib><creatorcontrib>Van Eck, Miranda</creatorcontrib><creatorcontrib>Hildebrand, Reeni B</creatorcontrib><creatorcontrib>van Wanrooij, Eva J.A</creatorcontrib><creatorcontrib>Kuiper, Johan</creatorcontrib><creatorcontrib>Maeda, Nobuyo</creatorcontrib><creatorcontrib>Benson, G Martin</creatorcontrib><creatorcontrib>Groot, Pieter H.E</creatorcontrib><creatorcontrib>Van Berkel, Theo J.C</creatorcontrib><title>Repopulation of Apolipoprotein E Knockout Mice With CCR2-Deficient Bone Marrow Progenitor Cells Does Not Inhibit Ongoing Atherosclerotic Lesion Development</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVE—Using bone marrow transplantation, we have previously demonstrated the critical role that hematopoietic CCR2 plays in early atherogenesis. Reconstitution of irradiated apolipoprotein (apo) E3–Leiden mice with CCR2-deficient bone marrow progenitor cells resulted in 86% reduction on overall atherosclerotic lesion development. However, no data on CCR2 in the cause of established atherosclerosis have been reported so far.
METHODS AND RESULTS—To study the role of CCR2 in established atherosclerotic lesions, bone marrow progenitor cells harvested from apoE and apoE/CCR2 mice were transplanted into lethally irradiated 16-week-old apoE mice with established atherosclerotic lesions. No significant differences were found in serum total cholesterol and triglycerides levels at different time points after transplantation. At age 16 weeks, lesion size in control apoE mice was 3.28±1.06×10 μm. At 9 weeks after transplantation, apoE→ apoE and apoE/CCR2→ apoE mice had developed significantly larger atherosclerotic lesions (4.49±0.92×10 μm, P<0.02 and 4.15±0.62×10 μm, P<0.04 compared with controls, respectively). However, no significant effect of disruption of hematopoietic CCR2 was observed on the progression of lesions. Furthermore, the macrophage positive area (78±4% versus 72±9%) and collagen content (11±6% versus 15±3%) of the lesions were similar as well.
CONCLUSION—In contrast to the critical role of CCR2 in the initiation of atherogenesis, bone marrow progenitor cell-derived CCR2 does not influence the progression of established atherosclerotic lesions, pointing to additional mechanisms for recruitment of monocytes at later stages of lesion development.</description><subject>Animals</subject><subject>Apolipoproteins E - genetics</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Atherosclerosis - immunology</subject><subject>Atherosclerosis - pathology</subject><subject>Atherosclerosis - therapy</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood vessels and receptors</subject><subject>Bone Marrow Transplantation</subject><subject>Cardiology. Vascular system</subject><subject>Cell Movement - drug effects</subject><subject>Cell Movement - immunology</subject><subject>Cholesterol - blood</subject><subject>Collagen - metabolism</subject><subject>Disease Progression</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hematopoietic Stem Cell Transplantation</subject><subject>Lymph Nodes - cytology</subject><subject>Lymph Nodes - immunology</subject><subject>Macrophages, Peritoneal - pathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Monocytes - pathology</subject><subject>Peritonitis - chemically induced</subject><subject>Peritonitis - immunology</subject><subject>Radiation Chimera</subject><subject>Receptors, CCR2</subject><subject>Receptors, Chemokine - genetics</subject><subject>T-Lymphocytes - immunology</subject><subject>Thioglycolates - pharmacology</subject><subject>Triglycerides - blood</subject><subject>Vertebrates: cardiovascular system</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkdFuFCEUhidGY2v1FQxp4uWMwMDsjHfrbNXGrTVN1UvCsIddWhamwLjxWXxZWXeThXAg5DvnP_AXxSXBFSENeY9JNb__WeE8SFOTllQMt11TMfqsOCecspI1dfM8n_GsK3nD6FnxKsaHzDNK8cvijPDZjHW4PS_-3sHox8nKZLxDXqP56K3JV8EnMA5doa_Oq0c_JXRjFKBfJm1Q39_RcgHaKAMuoY_eAbqRIfgd-h78GpxJPqAerI1o4SGibz6ha7cxg0no1q29cWs0TxsIPiqbYzIKLSHuW1jAb7B-3ObCr4sXWtoIb477RfHj09V9_6Vc3n6-7ufLUvGG1qUaWMtkp1RDZEtXHQxSMixppxmnGnNVD7StFVFk4AC402pFBqaVJHilSavri-LyUDc_-mmCmMSDn4LLkoLmH2s7yroMfThAKjcdA2gxBrOV4Y8gWOxtEZiIbIs42SL-2yIYzclvjwrTsIXVKfXoQwbeHQEZlbQ6SKdMPHHNrOWM8MyxA7fzNkGIj3baQRAbkDZt9tKsbjAvKcY8T4zLvGhd_wNe56hD</recordid><startdate>200505</startdate><enddate>200505</enddate><creator>Guo, Jian</creator><creator>de Waard, Vivian</creator><creator>Van Eck, Miranda</creator><creator>Hildebrand, Reeni B</creator><creator>van Wanrooij, Eva J.A</creator><creator>Kuiper, Johan</creator><creator>Maeda, Nobuyo</creator><creator>Benson, G Martin</creator><creator>Groot, Pieter H.E</creator><creator>Van Berkel, Theo J.C</creator><general>American Heart Association, Inc</general><general>Lippincott</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></search><sort><creationdate>200505</creationdate><title>Repopulation of Apolipoprotein E Knockout Mice With CCR2-Deficient Bone Marrow Progenitor Cells Does Not Inhibit Ongoing Atherosclerotic Lesion Development</title><author>Guo, Jian ; de Waard, Vivian ; Van Eck, Miranda ; Hildebrand, Reeni B ; van Wanrooij, Eva J.A ; Kuiper, Johan ; Maeda, Nobuyo ; Benson, G Martin ; Groot, Pieter H.E ; Van Berkel, Theo J.C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5623-cb484a9cc61a82d9ebaa40a29f452f05c3b283c1c1b5ee09fcd1b4fca10df18f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Apolipoproteins E - genetics</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Atherosclerosis - immunology</topic><topic>Atherosclerosis - pathology</topic><topic>Atherosclerosis - therapy</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood vessels and receptors</topic><topic>Bone Marrow Transplantation</topic><topic>Cardiology. Vascular system</topic><topic>Cell Movement - drug effects</topic><topic>Cell Movement - immunology</topic><topic>Cholesterol - blood</topic><topic>Collagen - metabolism</topic><topic>Disease Progression</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hematopoietic Stem Cell Transplantation</topic><topic>Lymph Nodes - cytology</topic><topic>Lymph Nodes - immunology</topic><topic>Macrophages, Peritoneal - pathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Monocytes - pathology</topic><topic>Peritonitis - chemically induced</topic><topic>Peritonitis - immunology</topic><topic>Radiation Chimera</topic><topic>Receptors, CCR2</topic><topic>Receptors, Chemokine - genetics</topic><topic>T-Lymphocytes - immunology</topic><topic>Thioglycolates - pharmacology</topic><topic>Triglycerides - blood</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Jian</creatorcontrib><creatorcontrib>de Waard, Vivian</creatorcontrib><creatorcontrib>Van Eck, Miranda</creatorcontrib><creatorcontrib>Hildebrand, Reeni B</creatorcontrib><creatorcontrib>van Wanrooij, Eva J.A</creatorcontrib><creatorcontrib>Kuiper, Johan</creatorcontrib><creatorcontrib>Maeda, Nobuyo</creatorcontrib><creatorcontrib>Benson, G Martin</creatorcontrib><creatorcontrib>Groot, Pieter H.E</creatorcontrib><creatorcontrib>Van Berkel, Theo J.C</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><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Jian</au><au>de Waard, Vivian</au><au>Van Eck, Miranda</au><au>Hildebrand, Reeni B</au><au>van Wanrooij, Eva J.A</au><au>Kuiper, Johan</au><au>Maeda, Nobuyo</au><au>Benson, G Martin</au><au>Groot, Pieter H.E</au><au>Van Berkel, Theo J.C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Repopulation of Apolipoprotein E Knockout Mice With CCR2-Deficient Bone Marrow Progenitor Cells Does Not Inhibit Ongoing Atherosclerotic Lesion Development</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2005-05</date><risdate>2005</risdate><volume>25</volume><issue>5</issue><spage>1014</spage><epage>1019</epage><pages>1014-1019</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>OBJECTIVE—Using bone marrow transplantation, we have previously demonstrated the critical role that hematopoietic CCR2 plays in early atherogenesis. Reconstitution of irradiated apolipoprotein (apo) E3–Leiden mice with CCR2-deficient bone marrow progenitor cells resulted in 86% reduction on overall atherosclerotic lesion development. However, no data on CCR2 in the cause of established atherosclerosis have been reported so far.
METHODS AND RESULTS—To study the role of CCR2 in established atherosclerotic lesions, bone marrow progenitor cells harvested from apoE and apoE/CCR2 mice were transplanted into lethally irradiated 16-week-old apoE mice with established atherosclerotic lesions. No significant differences were found in serum total cholesterol and triglycerides levels at different time points after transplantation. At age 16 weeks, lesion size in control apoE mice was 3.28±1.06×10 μm. At 9 weeks after transplantation, apoE→ apoE and apoE/CCR2→ apoE mice had developed significantly larger atherosclerotic lesions (4.49±0.92×10 μm, P<0.02 and 4.15±0.62×10 μm, P<0.04 compared with controls, respectively). However, no significant effect of disruption of hematopoietic CCR2 was observed on the progression of lesions. Furthermore, the macrophage positive area (78±4% versus 72±9%) and collagen content (11±6% versus 15±3%) of the lesions were similar as well.
CONCLUSION—In contrast to the critical role of CCR2 in the initiation of atherogenesis, bone marrow progenitor cell-derived CCR2 does not influence the progression of established atherosclerotic lesions, pointing to additional mechanisms for recruitment of monocytes at later stages of lesion development.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>15774908</pmid><doi>10.1161/01.ATV.0000163181.40896.42</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2005-05, Vol.25 (5), p.1014-1019 |
| issn | 1079-5642 1524-4636 |
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| subjects | Animals Apolipoproteins E - genetics Atherosclerosis (general aspects, experimental research) Atherosclerosis - immunology Atherosclerosis - pathology Atherosclerosis - therapy Biological and medical sciences Blood and lymphatic vessels Blood vessels and receptors Bone Marrow Transplantation Cardiology. Vascular system Cell Movement - drug effects Cell Movement - immunology Cholesterol - blood Collagen - metabolism Disease Progression Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Female Fundamental and applied biological sciences. Psychology Hematopoietic Stem Cell Transplantation Lymph Nodes - cytology Lymph Nodes - immunology Macrophages, Peritoneal - pathology Medical sciences Mice Mice, Knockout Monocytes - pathology Peritonitis - chemically induced Peritonitis - immunology Radiation Chimera Receptors, CCR2 Receptors, Chemokine - genetics T-Lymphocytes - immunology Thioglycolates - pharmacology Triglycerides - blood Vertebrates: cardiovascular system |
| title | Repopulation of Apolipoprotein E Knockout Mice With CCR2-Deficient Bone Marrow Progenitor Cells Does Not Inhibit Ongoing Atherosclerotic Lesion Development |
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