CoChat
Sign Up
Cited by 439

The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Increased Inflammatory Gene Expression in ABC Transporter–Deficient Macrophages: Free Cholesterol Accumulation, Increased Signaling via Toll-Like Receptors, and Neutrophil Infiltration of Atherosclerotic Lesions

Yvan-Charvet, Laurent, Welch, Carrie, Pagler, Tamara A., Ranalletta, Mollie, Lamkanfi, Mohamed, Han, Seongah, Ishibashi, Minako, Li, Rong, Wang, Nan, Tall, Alan R.·2008·Circulation
DOI 10.1161/circulationaha.108.793869PMC PMC2756536
Open this paper in CoChat — free account

Abstract

Background— Two macrophage ABC transporters, ABCA1 and ABCG1, have a major role in promoting cholesterol efflux from macrophages. Peritoneal macrophages deficient in ABCA1, ABCG1, or both show enhanced expression of inflammatory and chemokine genes. This study was undertaken to elucidate the mechanisms and consequences of enhanced inflammatory gene expression in ABC transporter–deficient macrophages. Methods and Results— Basal and lipopolysaccharide-stimulated thioglycollate-elicited peritoneal macrophages showed increased inflammatory gene expression in the order Abca1 −/− Abcg1 −/− > Abcg1 −/− > Abca1 −/− >wild-type. The increased inflammatory gene expression was abolished in macrophages deficient in Toll-like receptor 4 (TLR4) or MyD88/TRIF. TLR4 cell surface concentration was increased in Abca1 −/− Abcg1 −/− > Abcg1 −/− > Abca1 −/− > wild-type macrophages. Treatment of transporter-deficient cells with cyclodextrin reduced and cholesterol-cyclodextrin loading increased inflammatory gene expression. Abca1 −/− Abcg1 − bone marrow–derived macrophages showed enhanced inflammatory gene responses to TLR2, TLR3, and TLR4 ligands. To assess in vivo relevance, we injected intraperitoneally thioglycollate in Abcg1 −/− bone marrow–transplanted, Western diet–fed, Ldlr -deficient mice. This resulted in a profound inflammatory infiltrate in the adventitia and necrotic core region of atherosclerotic lesions, consisting primarily of neutrophils. Conclusions— The results suggest that high-density lipoprotein and apolipoprotein A-1 exert anti-inflammatory effects by promoting cholesterol efflux via ABCG1 and ABCA1 with consequent attenuation of signaling via Toll-like receptors. In response to a peripheral inflammatory stimulus, atherosclerotic lesions containing Abcg1 −/− macrophages experience an inflammatory “echo,” suggesting a possible mechanism of plaque destabilization in subjects with low high-density lipoprotein levels.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1161/circulationaha.108.793869

Cites

7 of 7 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

  • ABCA1 and ABCG1 modulate TLR signaling and efferocytosis, thereby indirectly shaping macrophage activation and inflammatory responses.

    “ABCA1 and ABCG1 modulate toll-like receptor (TLR) signaling and efferocytosis, thereby indirectly shaping macrophage activation and inflammatory responses28,29.”

    From Macrophage INSIG1 deficiency drives psoriasiform dermatitis via the SREBP2-STAT1 axis (2026) · cites this paper as [29]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 37

  1. 10.1073/pnas.91.20.9607 · DOI
  2. 10.1038/35018119 · DOI
  3. 10.1124/pr.58.3.1 · DOI
  4. 10.1074/jbc.M006738200 · DOI
  5. 10.1073/pnas.0403506101 · DOI
  6. 10.1161/01.atv.0000200082.58536.e1 · DOI
  7. 10.1194/jlr.M600218-JLR200 · DOI
  8. 10.1172/JCI32057 · DOI
  9. 10.1161/atvbaha.107.156935 · DOI
  10. Yvan-Charvet L, Ranalletta M, Wang N, Han S, Terasaka N, Li R, Welch C, Tall AR. Combined deficiency of ABCA1 and ABCG1 promotes foam cell accumulation and accelerates atherosclerosis in mice. J Clin Invest. 2007; 117: 3900–3908.
  11. 10.1194/jlr.M600428-JLR200 · DOI
  12. 10.1161/01.atv.0000166522.69552.99 · DOI
  13. 10.1016/j.cmet.2005.01.002 · DOI
  14. 10.4049/jimmunol.180.6.4273 · DOI
  15. 10.4049/jimmunol.180.5.3560 · DOI
  16. 10.1161/01.atv.0000240051.22944.dc · DOI
  17. 10.1161/01.atv.0000242275.92915.43 · DOI
  18. 10.1016/j.cmet.2006.02.008 · DOI
  19. 10.1128/iai.62.10.4304-4309.1994 · DOI
  20. 10.1161/01.atv.0000218998.75963.02 · DOI
  21. 10.1189/jlb.1206756 · DOI
  22. 10.1073/pnas.0704602104 · DOI
  23. 10.1016/S0022-2275(20)34940-3 · DOI
  24. 10.1083/jcb.127.5.1217 · DOI
  25. 10.2174/138161206778743501 · DOI
  26. 10.4049/jimmunol.164.7.3471 · DOI
  27. 10.1038/nm1008 · DOI · Paper page
  28. 10.1074/jbc.M801408200 · DOI
  29. 10.1242/jcs.115.12.2603 · DOI
  30. 10.1016/j.cell.2008.04.052 · DOI · Paper page
  31. Wolpe SD, Cerami A. Macrophage inflammatory protein 1 and 2: members of a novel supergene of cytokines. FASEB J. 1989; 3: 2765–2773.
  32. van Leeuwen M, Gijbels MJ, Duijvestijn A, Smook M, van de Gaar MJ, Heeringa P, de Winther MP, Tervaert JW. Accumulation of myeloperoxidase-positive neutrophils in atherosclerosis lesions in LDLR−/− mice. Arterioscler Thromb Vasc Biol. 2008; 28: 85–89.
  33. 10.1161/circresaha.107.160697 · DOI
  34. 10.1161/circulationaha.107.741181 · DOI · Paper page
  35. 10.1161/01.atv.0000156877.94472.a5 · DOI · Paper page
  36. 10.1038/ncpcardio0768 · DOI
  37. 10.1016/j.cmet.2008.03.001 · DOI · Paper page

Cited by

Sorted by citations

Metadata

Authors
Yvan-Charvet, L., Welch, C., Pagler, T. A., Ranalletta, M., Lamkanfi, M., Han, S., Ishibashi, M., Li, R., Wang, N., & Tall, A. R.
Affiliations
From the Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY (L.Y.-C., C.W., T.A.P., M.R., S.H., M.I., R.L., N.W., A.R.T.); and Department of Physiological Chemistry, Genentech, South San Francisco, Calif (M.L.).
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2008-10-28
Volume
118
Issue
18
Pages
1837-1847
ISSN
  • 0009-7322
  • 1524-4539
DOI
10.1161/circulationaha.108.793869
PMC
PMC2756536
Cited by
439
References
7
Language
en

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