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Cited by 88Cardiac Valve Diseases and TreatmentsAortic Disease and Treatment ApproachesCardiac Fibrosis and Remodeling

Progression of human aortic valve stenosis is associated with tenascin-C expression

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Satta, Jari, Melkko, Jukka, Pöllänen, Raimo, Tuukkanen, Juha, Pääkkö, Paavo, Ohtonen, Pasi, Mennander, Ari, Soini, Ylermi·2002·Journal of the American College of Cardiology
DOI 10.1016/s0735-1097(01)01705-3
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Abstract

Objectives We sought to assess tenascin-C (TN-C) expression and its possible pathobiological impact in human aortic valve stenosis.Background Tenascin-C, a large extracellular matrix glycoprotein, has lately been increasingly connected to cardiovascular pathologies. As TN-C is a multifunctional protein implicated in cell proliferation, migration and differentiation, we investigated the pattern of its expression in diseased human aortic valves.Methods Fifty-five tricuspid, non-rheumatic stenotic aortic valves were collected from patients undergoing aortic valve replacement, and the controls consisted of four normal valves from individuals who had suffered traumatic death and one from a patient operated on because of a noncalcified purely regurgitant valve. A monoclonal mouse antibody to human TN-C (143DB7) was used as the primary antibody in immunostaining. To study the source of TN-C messenger RNA synthesis, some tissue samples were also examined using in situ hybridization. In order to identify smooth muscle cell differentiation, commercially available antibodies against alpha-smooth muscle actin were used, and immunophenotypic analysis of inflammatory cells was carried out by using the monoclonal mouse antibodies UCHL-1, L26 and PGM-1.Results In normal valves, TN-C expression was associated with the basement membrane beneath the endothelial cells, whereas stenotic valves showed no such expression but rather immunoreactivity in the deeper layers of the valves. This reactivity was associated with the characteristics typical of the stenosing process and the increased mechanical loading caused by hypertension.Conclusions We hypothesize that the overexpression of TN-C in stenotic human aortic valves may emphasize that this disease is an active rather than a degenerative process.

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  • Increased production of extracellular matrix components, including periostin, tenascin, and proteoglycans, contributes to aortic valve remodelling during aortic stenosis.

    “In addition, the increased production of several components of the extracellular matrix, including periostin, tenascin (also called tenascin-c) and proteoglycans contributes to the remodelling of the aortic valve during AS35;36.”

    From Calcific aortic stenosis (2016) · cites this paper as [36]

    The Immunohistochemistry of TN-C and cellular composition section (page not specified in our copy) reports increased tenascin-C mRNA expression in stenotic valves, supporting the tenascin-C part of the claim. The paper does not establish increased periostin or proteoglycan production, and its discussion proposes rather than demonstrates that tenascin-C contributes to valve changes. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Many of the most differentially expressed genes in severe forms of CAVS were previously reported in smaller studies.

    “As expected, many of the most differentially expressed genes in severe forms of CAVS were previously reported in smaller studies (PDK4, BTG2, SLC16A9, GPR68, FAP, CNTFR, PLEKHS1, THY1, SCG2, CXCL5, TNC, TDO2, LINC01614).9,12,13,28, 29, 30, 31, 32, 33”

    From Transcriptomic signatures of calcific aortic valve stenosis severity in human tricuspid and bicuspid aortic valves (2025) · cites this paper as [32]

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Cites

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Research works printed but not linked: 2

  1. [8]8. Jones FS, Jones PL. The tenascin family of ECM glycoproteins: structure, function, and regulation during embryonic development and tissue remodelling. Dev Dyn 2000;218:235-59.
  2. [22]22. Gundersen D, Tran-Thang C, Sordat B. Plasmin-induced proteolysis of tenascin-C. J Immunol 1997;158:1051-60.

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Authors
Satta, J., Melkko, J., Pöllänen, R., Tuukkanen, J., Pääkkö, P., Ohtonen, P., Mennander, A., & Soini, Y.
Affiliations
Oulu University Hospital (FI)
Corresponding author
Satta, Jari
ORCID
Venue
Journal of the American College of Cardiology
Publisher
Elsevier BV
Published
2002-01
Volume
39
Issue
1
Pages
96-101
ISSN
0735-1097 (ISSN-L)
DOI
10.1016/s0735-1097(01)01705-3
OpenAlex
W2020797302
Cited by
88
References
23
Citations by year
2025: 4 · 2024: 3 · 2023: 2 · 2022: 1 · 2021: 7 · 2020: 4 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 4 · 2014: 1 · 2013: 3 · 2012: 5
FWCI
2.40
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of the American College of Cardiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Valve Diseases and Treatments
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Aortic Disease and Treatment Approaches
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords
tenascin-C, aortic stenosis, disease progression, extracellular matrix glycoprotein, tricuspid valve, hypertension, mechanical loading, basement membrane, smooth muscle differentiation, alpha-smooth muscle actin, inflammatory cells, aortic valve replacement
MeSH terms
Aged, Aged, 80 and over, Aortic Valve Stenosis, Female, Humans, Immunohistochemistry, Male, Middle Aged, Up-Regulation, In Situ Hybridization, Disease Progression, Tenascin

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