Ultrastructure of Early Lipid Accumulation in ApoE-Deficient Mice
Apolipoprotein (apo) E-deficient mice develop severe hypercholesterolemia and have lesions that progress from fatty streaks to fibrous plaques distributed in lesion-prone areas throughout the aorta. Lesions develop in apoE-deficient mice on a regular chow diet and will occur faster on a diet higher...
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Published in | Arteriosclerosis, thrombosis, and vascular biology Vol. 19; no. 4; pp. 847 - 853 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Philadelphia, PA
American Heart Association, Inc
01.04.1999
Hagerstown, MD Lippincott |
Subjects | |
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Abstract | Apolipoprotein (apo) E-deficient mice develop severe hypercholesterolemia and have lesions that progress from fatty streaks to fibrous plaques distributed in lesion-prone areas throughout the aorta. Lesions develop in apoE-deficient mice on a regular chow diet and will occur faster on a diet higher in cholesterol. Examination of the aortas from these mice on a chow diet by high-resolution, freeze-etch electron microscopy demonstrated lipid retention in the intima by 3 weeks of age. Lipid was retained in the matrix as individual particles between 33 and 48 nm in diameter, aligned along the collagen fibrils and in aggregates consisting of lipid particles with average diameters of 33 and 68 nm. Larger particles seemed to have formed from fusion of smaller particles. Lipid retention was more widespread in 5- and 9-week-old mice. Monocyte attachment to endothelial cells was observed by electron microscopy at 5 weeks of age. The appearance of the intimal lipid was similar to that previously described in rabbit models and suggests that lipid interaction with matrix filaments and subsequent aggregation of lipid particles are critical first steps in the process of foam cell formation. (Arterioscler Thromb Vasc Biol. 1999;19:847-853.) |
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AbstractList | Abstract
—Apolipoprotein (apo) E–deficient mice develop severe hypercholesterolemia and have lesions that progress from fatty streaks to fibrous plaques distributed in lesion-prone areas throughout the aorta. Lesions develop in apoE-deficient mice on a regular chow diet and will occur faster on a diet higher in cholesterol. Examination of the aortas from these mice on a chow diet by high-resolution, freeze-etch electron microscopy demonstrated lipid retention in the intima by 3 weeks of age. Lipid was retained in the matrix as individual particles between 33 and 48 nm in diameter, aligned along the collagen fibrils and in aggregates consisting of lipid particles with average diameters of 33 and 68 nm. Larger particles seemed to have formed from fusion of smaller particles. Lipid retention was more widespread in 5- and 9-week-old mice. Monocyte attachment to endothelial cells was observed by electron microscopy at 5 weeks of age. The appearance of the intimal lipid was similar to that previously described in rabbit models and suggests that lipid interaction with matrix filaments and subsequent aggregation of lipid particles are critical first steps in the process of foam cell formation. Apolipoprotein (apo) E-deficient mice develop severe hypercholesterolemia and have lesions that progress from fatty streaks to fibrous plaques distributed in lesion-prone areas throughout the aorta. Lesions develop in apoE-deficient mice on a regular chow diet and will occur faster on a diet higher in cholesterol. Examination of the aortas from these mice on a chow diet by high-resolution, freeze-etch electron microscopy demonstrated lipid retention in the intima by 3 weeks of age. Lipid was retained in the matrix as individual particles between 33 and 48 nm in diameter, aligned along the collagen fibrils and in aggregates consisting of lipid particles with average diameters of 33 and 68 nm. Larger particles seemed to have formed from fusion of smaller particles. Lipid retention was more widespread in 5- and 9-week-old mice. Monocyte attachment to endothelial cells was observed by electron microscopy at 5 weeks of age. The appearance of the intimal lipid was similar to that previously described in rabbit models and suggests that lipid interaction with matrix filaments and subsequent aggregation of lipid particles are critical first steps in the process of foam cell formation. Apolipoprotein (apo) E-deficient mice develop severe hypercholesterolemia and have lesions that progress from fatty streaks to fibrous plaques distributed in lesion-prone areas throughout the aorta. Lesions develop in apoE-deficient mice on a regular chow diet and will occur faster on a diet higher in cholesterol. Examination of the aortas from these mice on a chow diet by high-resolution, freeze-etch electron microscopy demonstrated lipid retention in the intima by 3 weeks of age. Lipid was retained in the matrix as individual particles between 33 and 48 nm in diameter, aligned along the collagen fibrils and in aggregates consisting of lipid particles with average diameters of 33 and 68 nm. Larger particles seemed to have formed from fusion of smaller particles. Lipid retention was more widespread in 5- and 9-week-old mice. Monocyte attachment to endothelial cells was observed by electron microscopy at 5 weeks of age. The appearance of the intimal lipid was similar to that previously described in rabbit models and suggests that lipid interaction with matrix filaments and subsequent aggregation of lipid particles are critical first steps in the process of foam cell formation. (Arterioscler Thromb Vasc Biol. 1999;19:847-853.) |
Author | Tamminen, M Breslow, J.L Qiao, J.H Mottino, G |
AuthorAffiliation | Received April 28, 1998; revision accepted July 31, 1998. From the Departments of Medicine (G.M., J.H.Q., J.S.F.) and Physiology (J.S.F.), UCLA School of Medicine, Los Angeles, Calif, and the Laboratory of Biochemical Genetics and Metabolism, The Rockefeller University (M.T., J.L.B.), New York, NY. Correspondence to Dr Joy S. Frank, Cardiovascular Research Laboratory, UCLA School of Medicine, MRL Building, Room 3780, 675 Circle Dr, Los Angeles, CA 90095-1760 |
AuthorAffiliation_xml | – name: Received April 28, 1998; revision accepted July 31, 1998. From the Departments of Medicine (G.M., J.H.Q., J.S.F.) and Physiology (J.S.F.), UCLA School of Medicine, Los Angeles, Calif, and the Laboratory of Biochemical Genetics and Metabolism, The Rockefeller University (M.T., J.L.B.), New York, NY. Correspondence to Dr Joy S. Frank, Cardiovascular Research Laboratory, UCLA School of Medicine, MRL Building, Room 3780, 675 Circle Dr, Los Angeles, CA 90095-1760 |
Author_xml | – sequence: 1 givenname: M surname: Tamminen fullname: Tamminen, M organization: Received April 28, 1998; revision accepted July 31, 1998. From the Departments of Medicine (G.M., J.H.Q., J.S.F.) and Physiology (J.S.F.), UCLA School of Medicine, Los Angeles, Calif, and the Laboratory of Biochemical Genetics and Metabolism, The Rockefeller University (M.T., J.L.B.), New York, NY. Correspondence to Dr Joy S. Frank, Cardiovascular Research Laboratory, UCLA School of Medicine, MRL Building, Room 3780, 675 Circle Dr, Los Angeles, CA 90095-1760 – sequence: 2 givenname: G surname: Mottino fullname: Mottino, G – sequence: 3 givenname: J.H surname: Qiao fullname: Qiao, J.H – sequence: 4 givenname: J.L surname: Breslow fullname: Breslow, J.L |
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Keywords | Pathogenesis Deficiency Rodentia Cardiovascular disease Metabolic diseases Lipids Hyperlipoproteinemia Foam cell Electron microscopy Vascular disease Pathology Vertebrata Mammalia Hypercholesterolemia Mouse Apolipoprotein E Animal Atherosclerosis Risk factor Dyslipemia |
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Snippet | Apolipoprotein (apo) E-deficient mice develop severe hypercholesterolemia and have lesions that progress from fatty streaks to fibrous plaques distributed in... Abstract —Apolipoprotein (apo) E–deficient mice develop severe hypercholesterolemia and have lesions that progress from fatty streaks to fibrous plaques... |
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SubjectTerms | Aging - pathology Animals Animals, Newborn - growth & development Animals, Newborn - metabolism Aorta - metabolism Aorta - ultrastructure Apolipoproteins E - deficiency Apolipoproteins E - genetics Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Female Lipid Metabolism Male Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Tunica Intima - metabolism Tunica Intima - ultrastructure |
Title | Ultrastructure of Early Lipid Accumulation in ApoE-Deficient Mice |
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