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Mixed allogeneic chimerism with wild‐type strains ameliorates atherosclerosis in apolipoprotein E‐deficient mice
Author(s) -
Ishimori Naoki,
Iwabuchi Kazuya,
Fujii Satoshi,
Watano Keiko,
Iwabuchi Chikako,
Ato Manabu,
Chiba Hitoshi,
Tanaka Shinya,
Kitabatake Akira,
Onoé Kazunori
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.69.5.732
Subject(s) - apolipoprotein e , bone marrow , biology , chimera (genetics) , apolipoprotein b , cholesterol , ratón , immunology , pathology , endocrinology , gene , medicine , biochemistry , disease
Atherosclerosis involves inflammatory processes between vasculartissues and hematocytes with a hyperlipidemic background. To examinewhether variations of hematocytes constitute one of the geneticcomponents in atherosclerosis, irradiated apolipoprotein E(apoE)‐deficient (apoE −/− ) mice with hypercholesterolemiaand preexisting atherosclerotic lesions were reconstituted withmixed bone marrow cells (BMC) from syngeneic and wild‐type(apoE +/+ ; atherosclerosis‐resistant SJL or ‐susceptibleB10.S) mice. Stable mixed allogeneic chimeras with small amounts ofserum apoE were established without any detrimentalcomplications. Compared with untreated apoE −/− miceor apoE −/− mice transplanted with syngeneic BMC alone, significant reduction of the cholesterol level and significant lesionregression were observed in the mixed chimeras. Furthermore, mixedchimeras given SJL BMC showed marked reductions in numbers of lesionscompared with those reconstituted with B10.S BMC. Cholesterol levels inthe former SJL chimeras, however, were significantly higher than thosein the latter B10.S chimeras. These findings indicate that theresistance of SJL to atherosclerosis resides in the bone marrow‐derivedcells.