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Br J Haematol ; 158(6): 788-97, 2012 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-22775554

RESUMO

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.


Assuntos
Anemia Falciforme/sangue , Plaquetas/metabolismo , Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/sangue , Adolescente , Adulto , Anemia Falciforme/complicações , Anemia Falciforme/tratamento farmacológico , Anemia Falciforme/genética , Anemia Falciforme/patologia , Biomarcadores , Endotélio Vascular/patologia , Feminino , Genótipo , Hemoglobina C/genética , Doença da Hemoglobina C/sangue , Doença da Hemoglobina C/genética , Humanos , Hidroxiureia/uso terapêutico , Mediadores da Inflamação/sangue , Masculino , Pessoa de Meia-Idade , Ativação Plaquetária , Membro 14 de Receptores do Fator de Necrose Tumoral/sangue , Traço Falciforme/sangue , Traço Falciforme/genética , Trombofilia/etiologia , Trombofilia/metabolismo , Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética , Membro 14 da Superfamília de Ligantes de Fatores de Necrose Tumoral/fisiologia , Adulto Jovem
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