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  • Title: The LDL receptor is the major pathway for beta-VLDL uptake by mouse peritoneal macrophages.
    Author: Perrey S, Ishibashi S, Kitamine T, Osuga J, Yagyu H, Chen Z, Shionoiri F, Iizuka Y, Yahagi N, Tamura Y, Ohashi K, Harada K, Gotoda T, Yamada N.
    Journal: Atherosclerosis; 2001 Jan; 154(1):51-60. PubMed ID: 11137082.
    Abstract:
    In order to determine the contribution of the low density lipoprotein receptor (LDL-R) to the removal of apoB-containing native lipoproteins by macrophages, we compared the uptake of beta-VLDL in peritoneal macrophages (MPM) from wild type mice and mice lacking the LDL-R. The d<1.006 g/ml lipoproteins obtained from apoE deficient mice fed a high fat diet were poorly degraded by macrophages and caused only a slight formation of CE in macrophages from both types of mice. On the other hand, d<1.006 g/ml lipoproteins obtained from LDL-R deficient mice fed a high fat diet, beta-VLDL with apoE, were avidly taken up by and markedly stimulated CE formation in wild type macrophages, but not in macrophages lacking the LDL-R. The degradation of 125I-labeled-apoE-containing beta-VLDL by wild type MPM was poorly inhibited by unlabeled human LDL, and beta-VLDL without apoE had no effects. In conclusion, we propose that the in vitro uptake of native apoE-enriched lipoproteins by murine macrophages is primarily mediated by the LDL receptor and not by other apoE-recognizing receptor systems such as: the LDL receptor related protein, the VLDL receptor or the triglyceride-rich lipoprotein receptor.
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