The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Decreased type II/type I TGF-beta receptor ratio in cells derived from human atherosclerotic lesions. Conversion from an antiproliferative to profibrotic response to TGF-beta1.
Open accessAbstract
Atherosclerosis and postangioplasty restenosis may result from abnormal wound healing. The present studies report that normal human smooth muscle cells are growth inhibited by TGF-beta1, a potent wound healing agent, and show little induction of collagen synthesis to TGF-beta1, yet cells grown from human vascular lesions are growth stimulated by TGF-beta1 and markedly increase collagen synthesis. Both cell types increase plasminogen activator inhibitor-1 production, switch actin phenotypes in response to TGF-beta1, and produce similar levels of TGF-beta activity. Membrane cross-linking of 125I-TGF-beta1 indicates that normal human smooth muscle cells express type I, II, and III receptors. The type II receptor is strikingly decreased in lesion cells, with little change in the type I or III receptors. RT-PCR confirmed that the type II TGF-beta1 receptor mRNA is reduced in lesion cells. Transfection of the type II receptor into lesion cells restores the growth inhibitory response to TGF-beta1, implying that signaling remains responsive. Because TGF-beta1 is overexpressed in fibroproliferative vascular lesions, receptor-variant cells would be allowed to grow in a slow, but uncontrolled fashion, while overproducing extracellular matrix components. This TGF-beta1 receptor dysfunction may be relevant for atherosclerosis, restenosis and related fibroproliferative diseases.
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.
Integrity signals
Registry
Cites
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.
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
Overall, C. M., Wrana, J. L., & Sodek, J. (1989) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)94267-5 · Cited by 636
Localization of PDGF-B Protein in Macrophages in All Phases of Atherogenesis
Ross, R., Masuda, J., Raines, E. W., Gown, A. M., Katsuda, S., Sasahara, M., Malden, L. T., Masuko, H., & Sato, H. (1990) · Science · doi:10.1126/science.2343305 · Cited by 574
Sato, Y., Tsuboi, R., Lyons, R., Moses, H., & Rifkin, D. B. (1990) · The Journal of cell biology · doi:10.1083/jcb.111.2.757 · Cited by 444
Janat, M. F., & Liau, G. (1992) · Journal of Cellular Physiology · doi:10.1002/jcp.1041500203 · Cited by 66
Cited by
Inducible Nitric Oxide Synthase and Inflammatory Diseases
Zamora, R., Vodovotz, Y., & Billiar, T. R. (2000) · Molecular Medicine · doi:10.1007/bf03401781 · Cited by 558
Disruption of TGF-β signaling in T cells accelerates atherosclerosis
Robertson, A.-K. L., Rudling, M., Zhou, X., Gorelik, L., Flavell, R. A., & Hansson, G. K. (2003) · Journal of Clinical Investigation · doi:10.1172/jci18607 · Cited by 441
Collagen synthesis in atherosclerosis: too much and not enough
Rekhter, M. (1999) · Cardiovascular Research · doi:10.1016/s0008-6363(98)00321-6 · Cited by 280
Grainger, D. J. (2004) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.0000114567.76772.33 · Cited by 277
Metadata
- Authors
- McCaffrey, T. A., Consigli, S., Du, B., Falcone, D. J., Sanborn, T. A., Spokojny, A. M., & Bush, H. L.
- Venue
- Journal of Clinical Investigation
- Published
- 1995-12-01
- Volume
- 96
- Issue
- 6
- Pages
- 2667-2675
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2072941419
- Cited by
- 167
- References
- 4
- FWCI
- 2.37
- Type
- journal article
- Language
- en
- Open access
- bronze
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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Decreased type II/type I TGF-beta receptor ratio in cells derived from human atherosclerotic lesions. Conversion from an antiproliferative to profibrotic response to TGF-beta1. https://app.cochat.ai/papers/10.1172/jci118333
- The paper
- McCaffrey, T. A., Consigli, S., Du, B., Falcone, D. J., Sanborn, T. A., Spokojny, A. M., & Bush, H. L. (1995). Decreased type II/type I TGF-beta receptor ratio in cells derived from human atherosclerotic lesions. Conversion from an antiproliferative to profibrotic response to TGF-beta1. Journal of Clinical Investigation. https://doi.org/10.1172/jci118333
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
