Transforming growth factor-beta1-mediated collagen gel contraction by cardiac fibroblasts
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TLDR
The aim of this study was to determine whether the ability of TGF-β1 to affect the contractile activity of cardiac fibroblasts depends on their differentiation into myofibroblast.About:
This article is published in American Journal of Hypertension.The article was published on 2004-05-01 and is currently open access. It has received 22 citations till now. The article focuses on the topics: Transforming growth factor & Fibroblast.read more
Citations
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Journal ArticleDOI
The role of α-smooth muscle actin in fibroblast-mediated matrix contraction and remodeling.
TL;DR: In this article, the role of α-SMA in fibroblast function using loss-and gain-of-function approaches was investigated. But α-sMA is not sufficient to promote contraction of the extracellular matrix.
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Cardiac fibroblast to myofibroblast differentiation in vivo and in vitro: Expression of focal adhesion components in neonatal and adult rat ventricular myofibroblasts
Jon-Jon Santiago,Aran L. Dangerfield,Sunil G. Rattan,Krista L. Bathe,Ryan H. Cunnington,Joshua E. Raizman,Kristen M. Bedosky,Darren H. Freed,Elissavet Kardami,Ian M.C. Dixon +9 more
TL;DR: C cultured neonatal and adult cardiac fibroblasts transition to myofibroblast in vitro and share expression profiles of cardiac my ofibroblast in vivo, and reduced motility with in vitro passage reflects enhanced production of focal adhesions.
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Transforming Growth Factor-β Receptor Type 1 (TGFβRI) Kinase Activity but Not p38 Activation Is Required for TGFβRI-Induced Myofibroblast Differentiation and Profibrotic Gene Expression
Ann M. Kapoun,Nicholas J. Gaspar,Ying Wang,Debby Damm,Yu-Wang Liu,Gilbert O'Young,Diana Quon,Andrew Lam,Kimberly Munson,Thomas-Toan Tran,Jing Ying Ma,Alison Murphy,Sundeep Dugar,Sarvajit Chakravarty,Andrew A. Protter,Fu-Qiang Wen,Xiangde Liu,Stephen I. Rennard,Linda S. Higgins +18 more
TL;DR: It is demonstrated that SD-208, but not SD-282, inhibited TGFβ-induced SMAD signaling, myofibroblast transformation, and collagen gel contraction, and these studies revealed that although the p38 pathway may not be needed for appearance or disappearance of the myofIBroblast, it can mediate a subset of inflammatory and fibrogenic events during the process of tissue repair and fibrosis.
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Reduced serum content and increased matrix stiffness promote the cardiac myofibroblast transition in 3D collagen matrices
TL;DR: The results suggest that reduced serum and increased matrix stiffness promote the myofibroblast phenotype in the myocardium, indicating the presence of positive feedback that may contribute to the pathogenesis of cardiac fibrosis.
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Deficiency of biglycan causes cardiac fibroblasts to differentiate into a myofibroblast phenotype
Ariane Melchior-Becker,Guang Dai,Zhaoping Ding,Liliana Schäfer,Jürgen Schrader,Marian F. Young,Jens W. Fischer +6 more
TL;DR: The data suggest that bgn deficiency promotes myofibroblast differentiation and proliferation in vitro and in vivo likely due to increased responses to TGF-β and SMAD2 signaling.
References
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A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding
TL;DR: This assay is very reproducible and rapid with the dye binding process virtually complete in approximately 2 min with good color stability for 1 hr with little or no interference from cations such as sodium or potassium nor from carbohydrates such as sucrose.
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Transforming growth factor-beta 1 induces alpha-smooth muscle actin expression in granulation tissue myofibroblasts and in quiescent and growing cultured fibroblasts.
TL;DR: It is shown that the subcutaneous administration of transforming growth factor- beta 1 to rats results in the formation of a granulation tissue in which alpha-SM actin expressing myofibroblasts are particularly abundant, suggesting that TGF beta 1 plays an important role in my ofibroblast differentiation during wound healing and fibrocontractive diseases by regulating the expression of alpha- SM actin in these cells.
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Alpha-Smooth Muscle Actin Expression Upregulates Fibroblast Contractile Activity
TL;DR: An increased alpha-SMA expression is sufficient to enhance fibroblast contractile activity, with the use of silicone substrates of different stiffness degrees.
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Collagen metabolism in cultured adult rat cardiac fibroblasts: response to angiotensin II and aldosterone.
TL;DR: A direct interaction between ALDO, AII and cardiac Fb in mediating myocardial fibrosis in hypertensive heart disease is suggested and this response appears to occur via type I corticoid receptors.
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Extracellular Matrix Remodeling in Heart Failure A Role for De Novo Angiotensin II Generation
TL;DR: ACE inhibition has proved effective in reducing mortal and morbid events, improving symptomatic status, and attenuating the progressive nature of cardiac failure in symptomatic patients with ventricular diastolic and/or systolic dysfunction in whom activation of the circulating RAAS is present as discussed by the authors.
Related Papers (5)
Transforming growth factor-beta 1-induced collagen production in cultures of cardiac fibroblasts is the result of the appearance of myofibroblasts.
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