CoChat
Sign Up
Cited by 27

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Anti-atherogenic effects of the acyl-CoA:cholesterol acyltransferase inhibitor, avasimibe (CI-1011), in cultured primary human macrophages

Rodriguez, Annabelle, Usher, David C·2002·Atherosclerosis
DOI 10.1016/s0021-9150(01)00620-7
Open this paper in CoChat — free account

Abstract

Acyl-CoA:cholesterol acyltransferase (ACAT) inhibitors have been shown to reduce atherosclerotic lesions in animals; however, the mechanism(s) for this effect remains unclear. Therefore, we used cultured primary human monocyte-derived macrophages (HMMs) to examine the effect of the ACAT inhibitor, avasimibe (CI-1011), during foam cell formation and during cholesterol efflux from established foam cells. To examine the effect of CI-1011 on foam cell development, HMMs were incubated with aggregated acetylated LDL (ag-acLDL)+/-CI-1011 for 48 h. Total cholesterol (TC) was 29% lower in HMMs incubated with ag-acLDL and CI-1011 compared with ag-acLDL (P<0.05). To determine if TC reduction was due to reduced ag-acLDL uptake by CI-1011, 125I-acLDL binding at 4 degrees C for 4 h to HMMs preincubated with acLDL or ag-acLDL, CI-1011, acLDL+CI-1011, or ag-acLDL+CI-1011 for 48 h was measured. Specific binding was 40% lower in cells preincubated with acLDL+CI-1011, 52% lower in cells preincubated with ag-acLDL+CI-1011 and 49% lower in cells preincubated with CI-1011 compared with cells preincubated with acLDL (P<0.0003). Because CI-1011 appeared to directly affect acLDL binding, 125I-acLDL (3-80 microg protein/ml) binding was done in HMMs preincubated with CI-1011 (0-10 microg/ml) for 48 h. The calculated B(max) decreased in HMMs exposed to increasing concentrations of CI-1011, suggesting that CI-1011 altered scavenger receptor function and/or number. To examine the effects of CI-1011 on cho…

Overview

Integrity signals

Registry

Crossref · 10.1016/s0021-9150(01)00620-7

Cites

1 of 1 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 21

  1. Rodriguez, 1999, Novel effects of the acyl-Coenzyme A:cholesterol acyltransferase inhibitor 58-035 on foam cell development in primary human monocyte-derived macrophages, Arterioscler. Thromb. Vasc. Biol., 19, 2199, 10.1161/01.ATV.19.9.2199 · DOI
  2. Meiner, 1996, Disruption of the acyl-CoA:cholesterol acyltransferase gene in mice: evidence suggesting multiple cholesterol esterification enzymes in mammals, Proc. Natl. Acad. Sci. USA, 93, 14041, 10.1073/pnas.93.24.14041 · DOI
  3. Lee, 1996, Inhibitors of acyl-CoA:cholesterol O-acyl transferase (ACAT) as hypocholesterolemic agents, J. Med. Chem., 39, 5031, 10.1021/jm960674d · DOI
  4. Ishii, 1998, Stimulation of cholesterol release from rabbit foam cells by the action of a new inhibitor for acyl CoA:cholesterol acyltransferase (ACAT), HL-004, J. Pharm. Exp. Ther., 287, 115
  5. Tanaka, 1994, Effect of the acyl-CoA:cholesterol acyltransferase inhibitor, E5324, on experimental atherosclerosis in rabbits, Atherosclerosis, 107, 187, 10.1016/0021-9150(94)90020-5 · DOI
  6. Sorbera, 1999, Avasimibe, treatment of lipoprotein disorders, Drugs Future, 24, 9, 10.1358/dof.1999.024.01.474029 · DOI
  7. Bocan, 2000, The ACAT inhibitor avasimibe reduces macrophages and matrix metalloproteinase expression in atherosclerotic lesions of hypercholesterolemic rabbits, Arterioscler. Thromb. Vasc. Biol., 20, 70, 10.1161/01.ATV.20.1.70 · DOI
  8. Havel, 1955, Distribution and chemical composition of ultracentrifugally separated lipoproteins in human serum, J. Clin. Invest., 34, 1345, 10.1172/JCI103182 · DOI
  9. Frankel-Conrat, 1957, Methods for investigating the essential groups for enzyme activity, Methods Enzymol., 4, 247, 10.1016/0076-6879(57)04059-8 · DOI
  10. Khoo, 1988, Enhanced macrophage uptake of low density lipoprotein after self-aggregation, Arteriosclerosis, 8, 348, 10.1161/01.ATV.8.4.348 · DOI
  11. Ishikawa, 1974, Quantitative analysis of cholesterol in 5 to 20 microliters of plasma, J. Lipid Res., 15, 286, 10.1016/S0022-2275(20)36809-7 · DOI
  12. Markwell, 1978, A modification of the Lowry procedure to simplify protein determination in membrane and lipoprotein samples, Anal. Biochem., 87, 206, 10.1016/0003-2697(78)90586-9 · DOI
  13. McFarlane, 1970, Short-term measurement of catabolic rates using iodine-labeled plasma proteins, J. Clin. Invest., 49, 1903, 10.1172/JCI106409 · DOI
  14. Bachorik, 1982, High affinity uptake and degradation of apolipoprotein E-free high density lipoprotein in cultured porcine hepatocytes, Biochemistry, 21, 4675, 10.1021/bi00265a044 · DOI
  15. Warner, 1995, Cell toxicity induced by inhibition of acyl Coenzyme A:cholesterol acyltransferase and accumulation of unesterified cholesterol, J. Biol. Chem., 270, 5772, 10.1074/jbc.270.11.5772 · DOI
  16. Zhang, 1996, Apolipoprotein E produced by human monocyte-derived macrophages mediates cholesterol efflux that occurs in the absence of added cholesterol acceptors, J. Biol. Chem., 271, 28641, 10.1074/jbc.271.45.28641 · DOI
  17. Kellner-Weibel, 1998, Effects of intracellular free cholesterol accumulation on macrophage viability, a model for foam cell death, Arterioscler. Thromb. Vasc. Biol., 18, 423, 10.1161/01.ATV.18.3.423 · DOI
  18. Kruth, 1994, Production of cholesterol-enriched nascent high density lipoproteins by human monocyte-derived macrophages is a mechanism that contributes to macrophage cholesterol efflux, J. Biol. Chem., 269, 24511, 10.1016/S0021-9258(19)51113-9 · DOI
  19. Zhang, 1997, Aggregated low density lipoprotein induces and enters surface-connected compartments of human monocyte macrophages, J. Biol. Chem., 272, 31700, 10.1074/jbc.272.50.31700 · DOI
  20. Kayden, 1985, The secretion of apolipoprotein E by human monocyte-derived macrophages, Arch. Biochem. Biophys., 239, 388, 10.1016/0003-9861(85)90704-0 · DOI
  21. Accad, 2000, Massive xanthomatosis and altered composition of atherosclerotic lesions in hyperlipidemic mice lacking acyl-CoA:cholesterol acyltransferase I, J. Clin. Invest., 105, 711, 10.1172/JCI9021 · DOI

Cited by

Sorted by citations

Metadata

Authors
Rodriguez, A., & Usher, D. C.
Venue
Atherosclerosis
Publisher
Elsevier BV
Published
2002-03
Volume
161
Issue
1
Pages
45-54
ISSN
0021-9150
DOI
10.1016/s0021-9150(01)00620-7
Cited by
27
References
1
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review