ArticleThe Journal of clinical investigation1998
Inhibition of norepinephrine-induced cardiac hypertrophy in s100beta transgenic mice.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 76 citations in OpenAlex.
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- Platelet tissue factor pathway inhibitor-α dampens cardiac thrombosis and associated fibrosis in mice.Journal of thrombosis and haemostasis : JTH · 2023Article
- RETRACTED: Therapeutic Potential of Mesenchymal Stem Cells versus Omega n - 3 Polyunsaturated Fatty Acids on Gentamicin-Induced Cardiac Degeneration.Pharmaceutics · 2022Article
- Association of S100B 3'UTR polymorphism with risk of chronic heart failure in a Chinese Han population.Medicine · 2020Article
- Correlation between Amitriptyline-Induced Cardiotoxic Effects and Cardiac S100b Protein in Isolated Rat Hearts.Balkan medical journal · 2016Article
- Article
- S100B protein in tissue development, repair and regeneration.World journal of biological chemistry · 2013Article
- S100B protein expression in the heart of deceased individuals by overdose: a new forensic marker?Clinics (Sao Paulo, Brazil) · 2012Article
- Intracellular and Extracellular Effects of S100B in the Cardiovascular Response to Disease.Cardiovascular psychiatry and neurology · 2010Article
- Article
- The AHNAKs are a class of giant propeller-like proteins that associate with calcium channel proteins of cardiomyocytes and other cells.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- The myocardial protein S100A1 plays a role in the maintenance of normal gene expression in the adult heart.Molecular and cellular biochemistry · 2003Article
- Impaired cardiac contractility response to hemodynamic stress in S100A1-deficient mice.Molecular and cellular biology · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have recently reported that the Ca2+-binding protein S100beta was induced in rat heart after infarction and forced expression of S100beta in neonatal rat cardiac myocyte cultures inhibited alpha1-adrenergic induction of beta myosin heavy chain (MHC) and skeletal alpha-actin (skACT). We now extend this work by showing that S100beta is induced in hearts of human subjects after myocardial infarction. Furthermore, to determine whether overexpression of S100beta was sufficient to inhibit in vivo hypertrophy, transgenic mice containing multiple copies of the human gene under the control of its own promoter, and CD1 control mice were treated with norepinephrine (NE) (1.5 mg/kg) or vehicle, intraperitoneally twice daily for 15 d. In CD1, NE produced an increase in left ventricular/body weight ratio, ventricular wall thickness, induction of skACT, atrial natriuretic factor, betaMHC, and downregulation of alphaMHC. In transgenic mice, NE induced S100beta transgene mRNA and protein, but provoked neither hypertrophy nor regulated cardiac-specific gene expression. NE induced hypertrophy in cultured CD1 but not S100beta transgenic myocytes, confirming that the effects of S100beta on cardiac mass reflected myocyte-specific responses. These transgenic studies complement in vitro data and support the hypothesis that S100beta acts as an intrinsic negative regulator of the myocardial hypertrophic response.
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