Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/200098
Type: Artigo de periódico
Title: Elevated Plasma Levels And Platelet-associated Expression Of The Pro-thrombotic And Pro-inflammatory Protein, Tnfsf14 (light), In Sickle Cell Disease.
Author: Garrido, Vanessa T
Proença-Ferreira, Renata
Dominical, Venina M
Traina, Fabiola
Bezerra, Marcos A C
de Mello, Mariana R B
Colella, Marina P
Araújo, Aderson S
Saad, Sara T O
Costa, Fernando F
Conran, Nicola
Abstract: Chronic vascular inflammation and endothelial activation may initiate vaso-occlusion in sickle cell disease (SCD). TNFSF14 (CD258; LIGHT), a recently-identified pro-thrombotic and pro-inflammatory tumour necrosis factor (TNF)-superfamily cytokine, has a potent activating effect on endothelial cells. We evaluated whether TNFSF14 production is altered in SCD and whether platelets contribute to this production. TNFSF14 was measured in platelet-free plasma from healthy-control individuals (CON), steady-state sickle cell anaemia (SCA), SCA on hydroxycarbamide therapy (SCAHC) and haemoglobin SC (HbSC) patients. Mean plasma TNFSF14 was significantly increased in SCA, SCAHC and HbSC, compared to CON individuals. In SCA/SCAHC patients, plasma TNFSF14, showed no correlation with haematological variables, but was significantly correlated with serum lactate dehydrogenase and inflammatory markers (CD40LG , IL8 and ICAM1). Platelet-membrane TNFSF14 expression was significantly augmented on SCA platelets, and correlated with platelet activation; furthermore, measurement of platelet TNFSF14 release indicated that platelets may be a major source of circulating TNFSF14 in SCA. Interestingly, high plasma TNFSF14 was significantly associated with elevated tricuspid regurgitant velocity (≥2·5 m/s) in a population of SCA/SCAHC patients. The pro-inflammatory and atherogenic cytokine, TNFSF14, could contribute to endothelial activation and inflammation in SCA; future investigations may confirm whether this protein contributes to major clinical complications of the disease, such as pulmonary hypertension, and represents a potential therapeutic target.
Subject: Adolescent
Adult
Anemia, Sickle Cell
Biological Markers
Blood Platelets
Endothelium, Vascular
Female
Genotype
Hemoglobin C
Hemoglobin C Disease
Humans
Hydroxyurea
Inflammation Mediators
Male
Middle Aged
Platelet Activation
Receptors, Tumor Necrosis Factor, Member 14
Sickle Cell Trait
Thrombophilia
Tumor Necrosis Factor Ligand Superfamily Member 14
Young Adult
Rights: fechado
Identifier DOI: 10.1111/j.1365-2141.2012.09218.x
Address: http://www.ncbi.nlm.nih.gov/pubmed/22775554
Date Issue: 2012
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

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