2001
DOI: 10.1093/ndt/16.2.361
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Plasma transforming growth factor β1 and platelet activation: implications for studies in transplant recipients

Abstract: To avoid erroneous hypotheses concerning TGF beta(1) and perpetuating confusion in the literature over levels in health and disease, it is imperative that proper internal controls for platelet activation are used. The effects of experimental treatments and drugs on platelet biology must be rigorously controlled when attempting to measure and interpret plasma levels of TGF beta(1) in clinical practice.

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Cited by 21 publications
(15 citation statements)
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“…In vivo, conservative values for total TGF-β 1 levels obtained from healthy subjects were reported to be ≤500 pg/mL. 43,44 When assuming a ratio of 10 for total versus active TGF-β 1 , 45 this corresponds to concentrations of active TGF-β 1 ≤50 pg/mL (ie, to concentrations that did not yet affect conduction and automaticity in the fibrosis models of this study). However, slight elevations of TGF-β 1 above this value slowed conduction and increased ectopic activity, indicating a narrow margin of safety that may be readily overcome in vivo in situations of increased TGF-β 1 secretion as is generally the case during cardiac fibrotic remodeling and in patients with coronary heart disease.…”
Section: Relevance For the Intact Heartmentioning
confidence: 86%
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“…In vivo, conservative values for total TGF-β 1 levels obtained from healthy subjects were reported to be ≤500 pg/mL. 43,44 When assuming a ratio of 10 for total versus active TGF-β 1 , 45 this corresponds to concentrations of active TGF-β 1 ≤50 pg/mL (ie, to concentrations that did not yet affect conduction and automaticity in the fibrosis models of this study). However, slight elevations of TGF-β 1 above this value slowed conduction and increased ectopic activity, indicating a narrow margin of safety that may be readily overcome in vivo in situations of increased TGF-β 1 secretion as is generally the case during cardiac fibrotic remodeling and in patients with coronary heart disease.…”
Section: Relevance For the Intact Heartmentioning
confidence: 86%
“…46 This may be due, at least in part, to problems associated with the reliable determination of TGF-β 1 plasma levels. 43,44 If these difficulties can be overcome and if methodologies are conceived which permit investigations of electrotonic interactions between myofibroblasts and cardiomyocytes in vivo, plasma levels of TGF-β 1 may eventually turn into a meaningful biomarker for hearts at risk for arrhythmias. Moreover, TGF-β 1 -regulated ion channels may emerge as new targets in antiarrhythmic therapies that circumvent known problems associated with general suppression of TGF-β 1 signaling.…”
Section: Relevance For the Intact Heartmentioning
confidence: 99%
“…Unfortunately, only one of these studies investigated TGF β 1 GCF levels in health and neither demonstrated how these levels relate to systemic TGF β 1 levels. This is important because both studies indicated that concentrations of the growth factor in GCF were between 40 and 100‐fold greater than values reported in the literature for plasma (Coupes et al , 2001).…”
Section: Introductionmentioning
confidence: 85%
“…However, serum levels of the growth factor may reflect not only renal produced, but also platelet-derived TGF-β 1 after platelet degranulation. Thus, estimation of platelet activation in the blood samples is necessary [15]. …”
Section: Introductionmentioning
confidence: 99%