ArticleThe American journal of pathology2011
Transforming growth factor-β regulates the growth of valve interstitial cells in vitro.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Tricuspid Valve Is Transcriptionally Active During Prolonged Pressure Overload, Right-Sided Heart Failure, and Valve Regurgitation.Journal of the American Heart Association · 2026Article
- Plasma Proteomic Assessment of Calcific Aortic Valve Disease in Older Adults.Journal of the American Heart Association · 2025Article
- Macrophages as key modulators of calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025Review
- TGFβ2 and TGFβ3 mediate appropriate context-dependent phenotype of rat valvular interstitial cells.iScience · 2021Article
- Tumor necrosis factor-α promotes and exacerbates calcification in heart valve myofibroblast populations.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- The effect of physiological stretch and the valvular endothelium on mitral valve proteomes.Experimental biology and medicine (Maywood, N.J.) · 2019Article
- FGF-2 inhibits contractile properties of valvular interstitial cell myofibroblasts encapsulated in 3D MMP-degradable hydrogels.APL bioengineering · 2018Article
- Dysregulation of hyaluronan homeostasis during aortic valve disease.Matrix biology : journal of the International Society for Matrix Biology · 2017Article
- Fibroblast growth factor 9 (FGF9) regulation of cyclin D1 and cyclin-dependent kinase-4 in ovarian granulosa and theca cells of cattle.Molecular and cellular endocrinology · 2017Article
- Role of cell-matrix interactions on VIC phenotype and tissue deposition in 3D PEG hydrogels.Journal of tissue engineering and regenerative medicine · 2016Article
- Inflammation Drives Retraction, Stiffening, and Nodule Formation via Cytoskeletal Machinery in a Three-Dimensional Culture Model of Aortic Stenosis.The American journal of pathology · 2016Article
- Involvement of Immune Cell Network in Aortic Valve Stenosis: Communication between Valvular Interstitial Cells and Immune Cells.Immune network · 2016Review
- Mitral valve disease--morphology and mechanisms.Nature reviews. Cardiology · 2015Review
- TGF-β signalling and reactive oxygen species drive fibrosis and matrix remodelling in myxomatous mitral valves.Cardiovascular research · 2013Article
- Sex-related differences in gene expression by porcine aortic valvular interstitial cells.PloS one · 2012Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Although valve interstitial cell (VIC) growth is an essential feature of injured and diseased valves, the regulation of VIC growth is poorly understood. Transforming growth factor (TGF)-β promotes VIC proliferation in early-stage wound repair; thus, herein, we tested the hypothesis that TGF-β regulates VIC proliferation under normal nonwound conditions using low-density porcine VIC monolayers. Cell numbers were counted during a 10-day period, whereas proliferation and apoptosis were quantified by bromodeoxyuridine staining and TUNEL, respectively. The extent of retinoblastoma protein phosphorylation and expression of cyclin D1, CDK 4, and p27 were compared using Western blot analysis. Adhesion was quantified using a trypsin adhesion assay, and morphological change was demonstrated by immunofluorescence localization of α-smooth muscle actin and vinculin. TGF-β-treated VICs were rhomboid; significantly decreased in number, proliferation, and retinoblastoma protein phosphorylation; and concomitantly had decreased expression of cyclin D1/CDK4 and increased expression of p27. TGF-β-treated VICs adhered better to substratum and had more vinculin plaques and α-smooth muscle actin stress fibers than did controls. Thus, the regulation of VIC growth by TGF-β is context dependent. TGF-β prevents excessive heart valve growth under normal physiological conditions while it promotes cell proliferation in the early stages of repair, when increased VICs are required.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.