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Citations to this article

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.
T A McCaffrey, … , A M Spokojny, H L Bush Jr
T A McCaffrey, … , A M Spokojny, H L Bush Jr
Published December 1, 1995
Citation Information: J Clin Invest. 1995;96(6):2667-2675. https://doi.org/10.1172/JCI118333.
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Research Article Article has an altmetric score of 3

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.

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Abstract

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.

Authors

T A McCaffrey, S Consigli, B Du, D J Falcone, T A Sanborn, A M Spokojny, H L Bush Jr

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Total citations by year

Year: 2023 2022 2021 2020 2019 2018 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 2004 2003 2002 2001 2000 1999 1998 1997 1996 Total
Citations: 1 1 2 2 1 2 2 3 3 1 3 3 1 9 3 1 3 1 4 5 9 16 17 17 14 4 2 130
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Citations to this article in year 2009 (9)

Title and authors Publication Year
Cardiovascular inflammation and lesion cell apoptosis: a novel connection via the interferon-inducible immunoproteasome
Z Yang, D Gagarin, GS 3rd, N Hammell, I Toma, CA Hu, A Iwasa, TA McCaffrey
Arteriosclerosis, thrombosis, and vascular biology 2009
Protein kinase C delta mediates arterial injury responses through regulation of vascular smooth muscle cell apoptosis
D Yamanouchi, K Kato, EJ Ryer, F Zhang, B Liu
Cardiovascular Research 2009
Arterial gene transfer of the TGF-beta signalling protein Smad3 induces adaptive remodelling following angioplasty: a role for CTGF
R Kundi, ST Hollenbeck, D Yamanouchi, BC Herman, R Edlin, EJ Ryer, C Wang, S Tsai, B Liu, KC Kent
Cardiovascular Research 2009
TGF-beta through Smad3 signaling stimulates vascular smooth muscle cell proliferation and neointimal formation
S Tsai, ST Hollenbeck, EJ Ryer, R Edlin, D Yamanouchi, R Kundi, C Wang, B Liu, KC Kent
American journal of physiology. Heart and circulatory physiology 2009
Transforming growth factor-β1 induces matrix metalloproteinase-9 expression in human meningeal cells via ERK and Smad pathways
T Okamoto, S Takahashi, E Nakamura, K Nagaya, T Hayashi, K Fujieda
Biochemical and Biophysical Research Communications 2009
Effect of Cytomodulin-10 (TGF-ß1 analogue) on wound healing by primary intention in a murine model
S Basu, M Kumar, JP Chansuria, TB Singh, R Bhatnagar, VK Shukla
International Journal of Surgery 2009
El papel esencial de la vía TGFβ/Smad en la regulación de las células de músculo liso vasculares dependiente de las estatinas
C Rodríguez
Clínica e Investigación en Arteriosclerosis 2009
TGF-β through Smad3 signaling stimulates vascular smooth muscle cell proliferation and neointimal formation
S Tsai, ST Hollenbeck, EJ Ryer, R Edlin, D Yamanouchi, R Kundi, C Wang, B Liu, KC Kent
American journal of physiology. Heart and circulatory physiology 2009
Established neointimal hyperplasia in vein grafts expands via TGF-β-mediated progressive fibrosis
Z Jiang, M Tao, KA Omalley, D Wang, CK Ozaki, SA Berceli
American journal of physiology. Heart and circulatory physiology 2009

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