Increased Atherosclerosis in Hyperlipidemic Mice Deficient in α-Tocopherol Transfer Protein and Vitamin E
Although lipid peroxidation in the subendothelial space has been hypothesized to play a central role in atherogenesis, the role of vitamin E in preventing lipid peroxidation and lesion development remains uncertain. Here we show that in atherosclerosis-susceptible apolipoprotein E knockout mice, vit...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2000-12, Vol.97 (25), p.13830-13834 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Terasawa, Y Ladha, Z Leonard, S W Morrow, J D Newland, D Sanan, D Packer, L Traber, M G Farese, Jr, R V |
| description | Although lipid peroxidation in the subendothelial space has been hypothesized to play a central role in atherogenesis, the role of vitamin E in preventing lipid peroxidation and lesion development remains uncertain. Here we show that in atherosclerosis-susceptible apolipoprotein E knockout mice, vitamin E deficiency caused by disruption of the α-tocopherol transfer protein gene (Ttpa) increased the severity of atherosclerotic lesions in the proximal aorta. The increase was associated with increased levels of isoprostanes, a marker of lipid peroxidation, in aortic tissue. These results show that vitamin E deficiency promotes atherosclerosis in a susceptible setting and support the hypothesis that lipid peroxidation contributes to lesion development. Ttpa-/-mice are a genetic model of vitamin E deficiency and should be valuable for studying other diseases in which oxidative stress is thought to play a role. |
| doi_str_mv | 10.1073/pnas.240462697 |
| format | Article |
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Here we show that in atherosclerosis-susceptible apolipoprotein E knockout mice, vitamin E deficiency caused by disruption of the α-tocopherol transfer protein gene (Ttpa) increased the severity of atherosclerotic lesions in the proximal aorta. The increase was associated with increased levels of isoprostanes, a marker of lipid peroxidation, in aortic tissue. These results show that vitamin E deficiency promotes atherosclerosis in a susceptible setting and support the hypothesis that lipid peroxidation contributes to lesion development. 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Here we show that in atherosclerosis-susceptible apolipoprotein E knockout mice, vitamin E deficiency caused by disruption of the α-tocopherol transfer protein gene (Ttpa) increased the severity of atherosclerotic lesions in the proximal aorta. The increase was associated with increased levels of isoprostanes, a marker of lipid peroxidation, in aortic tissue. These results show that vitamin E deficiency promotes atherosclerosis in a susceptible setting and support the hypothesis that lipid peroxidation contributes to lesion development. Ttpa-/-mice are a genetic model of vitamin E deficiency and should be valuable for studying other diseases in which oxidative stress is thought to play a role.</description><subject>a-tocopherol transfer protein</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Aorta</subject><subject>Arteriosclerosis - complications</subject><subject>Arteriosclerosis - genetics</subject><subject>Arteriosclerosis - pathology</subject><subject>Atherosclerosis</subject><subject>Base Sequence</subject><subject>Biological Sciences</subject><subject>Carrier Proteins - genetics</subject><subject>Cholesterols</subject><subject>DNA Primers</subject><subject>Hyperlipidemias - complications</subject><subject>Hyperlipidemias - genetics</subject><subject>Lesions</subject><subject>Lipid Peroxidation</subject><subject>Lipids</subject><subject>Lipoproteins</subject><subject>Medical research</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Ttpa gene</subject><subject>Vitamin E</subject><subject>Vitamin E deficiency</subject><subject>Vitamin E Deficiency - complications</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0ctu1DAUBmALgehQ2LJCELGousngu2OJTVVKW6kIFgNby-OcUI-SOLUTRB-LF-GZ6jDDcFnAxrZ0vt869kHoKcFLghV7NfQ2LSnHXFKp1T20IFiTUnKN76MFxlSVFaf8AD1KaYMx1qLCD9EByUooohZoc9m7CDZBXZyM1xBDcu28-lT4vri4HSC2fvA1dN4V77yD4g003nnoxxl8_1auggvDnGyLVbR9aiAWH2IYIZdtXxef_Gi7fD57jB40tk3wZLcfoo9vz1anF-XV-_PL05Or0gmKx1JaTknNRFVzwZhs6ooCE05bjq0lQvJKrwlwaiUIZyshHWNEU8LWTFgNjB2i19t7h2ndQe1yq9G2Zoi-s_HWBOvNn5XeX5vP4YshSkqS40e7eAw3E6TRdD45aFvbQ5iSUZQLqXj1X0iUYkoTmuHLv-AmTLHPf2AoJoxW5AdabpHLv58iNPuGCTbzqM08arMfdQ48__2Zv_huthm82IE5-LOslaHCEFYxnMXxv4VpprYd4euY6bMt3aQxxL2lUkouBLsDU8nHwg</recordid><startdate>20001205</startdate><enddate>20001205</enddate><creator>Terasawa, Y</creator><creator>Ladha, Z</creator><creator>Leonard, S W</creator><creator>Morrow, J D</creator><creator>Newland, D</creator><creator>Sanan, D</creator><creator>Packer, L</creator><creator>Traber, M G</creator><creator>Farese, Jr, R V</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</general><general>National Academy of Sciences</general><general>The National Academy of Sciences</general><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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20001205</creationdate><title>Increased Atherosclerosis in Hyperlipidemic Mice Deficient in α-Tocopherol Transfer Protein and Vitamin E</title><author>Terasawa, Y ; 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| subjects | a-tocopherol transfer protein Animals Antioxidants Aorta Arteriosclerosis - complications Arteriosclerosis - genetics Arteriosclerosis - pathology Atherosclerosis Base Sequence Biological Sciences Carrier Proteins - genetics Cholesterols DNA Primers Hyperlipidemias - complications Hyperlipidemias - genetics Lesions Lipid Peroxidation Lipids Lipoproteins Medical research Mice Mice, Inbred C57BL Mice, Knockout Proteins Rodents Ttpa gene Vitamin E Vitamin E deficiency Vitamin E Deficiency - complications |
| title | Increased Atherosclerosis in Hyperlipidemic Mice Deficient in α-Tocopherol Transfer Protein and Vitamin E |
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