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Titolo:
Plasma transforming growth factor beta(1) and platelet activation: implications for studies in transplant recipients
Autore:
Coupes, BM; Williams, S; Roberts, ISD; Short, CD; Brenchley, PEC;
Indirizzi:
Manchester Royal Infirm, Manchester Inst Nephrol & Transplantat, Renal ResLabs, Manchester M13 9WL, Lancs, England Manchester Royal Infirm Manchester Lancs England M13 9WL , Lancs, England Univ Manchester, Lab Med Acad Grp, Manchester M13 9PL, Lancs, England UnivManchester Manchester Lancs England M13 9PL M13 9PL, Lancs, England
Titolo Testata:
NEPHROLOGY DIALYSIS TRANSPLANTATION
fascicolo: 2, volume: 16, anno: 2001,
pagine: 361 - 367
SICI:
0931-0509(200102)16:2<361:PTGFBA>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
RENAL-ALLOGRAFT RECIPIENTS; TGF-BETA; CYCLOSPORINE; BLOOD; GROWTH-FACTOR-BETA-1; AGGREGATION; TGF-BETA-1; EXPRESSION;
Keywords:
immunosuppression; platelets; renal allografts; TGF ss(1); immunoassay;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Brenchley, PEC Manchester Royal Infirm, Manchester Inst Nephrol & Transplantat, Renal ResLabs, Oxford Rd, Manchester M13 9WL, Lancs, England Manchester Royal Infirm Oxford Rd Manchester Lancs England M13 9WL
Citazione:
B.M. Coupes et al., "Plasma transforming growth factor beta(1) and platelet activation: implications for studies in transplant recipients", NEPH DIAL T, 16(2), 2001, pp. 361-367

Abstract

Background. Evidence from animal models supports the hypothesis that dysregulated transforming growth factor beta (1) (TGF beta (1)) expression playsa role in chronic allograft rejection, the progression of diabetic nephropathy and fibrotic glomerulopathies. However, more evidence is required to support this hypothesis in man, and the current literature concerning blood TGF beta (1) levels in clinical studies is highly confused. We have investigated: (i) the hypothesis that the widespread practice of activating clinical samples Drier to measurement of TGF beta (1) is detecting the platelet-released pool of TGF beta (1), artefactually generated on venepuncture and unrepresentative of the real circulating in vivo TGF beta (1) pool; and (ii)the effect of different immunosuppressive drugs on apparent TGF beta (1) plasma levels. Methods. The effect of two different venepuncture procedures on plasma TGFbeta (1) was compared in 10 healthy volunteers, one procedure designed to minimize platelet activation and the other representing standard venepuncture practice in a clinic situation. Blood samples from 52 renal transplant recipients on either cyclosporine or tacrolimus immunosuppression were takenby standard venepuncture to investigate the effect of immunosuppressive drugs on plasma TGF beta (1). Plasma TGF beta (1) and beta thromboglobulin were measured by ELISA. Results, Among 10 healthy volunteers who underwent two different methods of venepuncture, eight of 10 had undetectable levels of TGF beta (1) (<100 pg/ml) under conditions that: minimize platelet activation. In contrast, all10 paired plasma samples collected by vacutainer had measurable TGF<beta>(1) (median 7.70 ng/ml, interquartile range 5.87-13.64 ng/ml) following acid/urea activation. The median beta TG level(a measure of platelet degranulation) was 0.71 mug/ml (interquartile range 0.53-1.19 mug/ml) in the special collections compared with 3.39 mug/ml (interquartile range 2.27-4.33 mug/ml) in the vacutainer samples (P = 0.0029). Among 52 allograft recipients there was a significantly higher mean TGF beta (1) level in plasma from patients on cyclosporine therapy compared with patients on tacrolimus (28090 +/- 26860 pg/ml vs 7173 +/- 10610 pg/ml, respectively; P < 0.002). Mean plasma <beta>TG levels were also significantly higher during cyclosporine therapy compared with tacrolimus (8.14 +/- 5.54 mug/ml vs 3.66 +/- 3.32 mug/ml, respectively; P < 0.002). However, when TGF<beta>(1) values were corrected forthe degree of platelet activation (by factoring with beta TG) there was nosignificant difference between TGF beta (1) levels on cyclosporine or tacrolimus (4117 +/- 2993 pg/mug beta TG vs 2971 +/- 658 pg/mug beta TG respectively; P = 0.294). Conclusions, To avoid erroneous hypotheses concerning TGF beta (1) and perpetuating confusion in the literature over levels in health and disease, itis 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 plasmalevels of TGF beta (1) in clinical practice.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 11:27:43