{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T13:26:16Z","timestamp":1791033976964,"version":"4.1.0"},"reference-count":34,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2012,7,6]],"date-time":"2012-07-06T00:00:00Z","timestamp":1341532800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Br J Haematol"],"published-print":{"date-parts":[[2012,9]]},"abstract":"Summary<\/jats:title>\n \n Chronic vascular inflammation and endothelial activation may initiate vaso\u2010occlusion in sickle cell disease (\n SCD<\/jats:styled-content>\n ).\n TNFSF<\/jats:styled-content>\n 14 (\n CD<\/jats:styled-content>\n 258;\n LIGHT<\/jats:styled-content>\n ), a recently\u2010identified pro\u2010thrombotic and pro\u2010inflammatory tumour necrosis factor (\n TNF<\/jats:styled-content>\n )\u2010superfamily cytokine, has a potent activating effect on endothelial cells. We evaluated whether\n TNFSF<\/jats:styled-content>\n 14 production is altered in\n SCD<\/jats:styled-content>\n and whether platelets contribute to this production.\n TNFSF<\/jats:styled-content>\n 14 was measured in platelet\u2010free plasma from healthy\u2010control individuals (\n CON<\/jats:styled-content>\n ), steady\u2010state sickle cell anaemia (\n SCA<\/jats:styled-content>\n ),\n SCA<\/jats:styled-content>\n on hydroxycarbamide therapy (\n SCAHC<\/jats:styled-content>\n ) and haemoglobin\n SC<\/jats:styled-content>\n (Hb\n SC<\/jats:styled-content>\n ) patients. Mean plasma\n TNFSF<\/jats:styled-content>\n 14 was significantly increased in\n SCA<\/jats:styled-content>\n ,\n SCAHC<\/jats:styled-content>\n and Hb\n SC<\/jats:styled-content>\n , compared to\n CON<\/jats:styled-content>\n individuals. In\n SCA<\/jats:styled-content>\n \/\n SCAHC<\/jats:styled-content>\n patients, plasma\n TNFSF<\/jats:styled-content>\n 14, showed no correlation with haematological variables, but was significantly correlated with serum lactate dehydrogenase and inflammatory markers (\n CD<\/jats:styled-content>\n 40\n LG<\/jats:styled-content>\n ,<\/jats:italic>\n IL<\/jats:styled-content>\n 8 and\n ICAM<\/jats:styled-content>\n 1). Platelet\u2010membrane\n TNFSF<\/jats:styled-content>\n 14 expression was significantly augmented on\n SCA<\/jats:styled-content>\n platelets, and correlated with platelet activation; furthermore, measurement of platelet\n TNFSF<\/jats:styled-content>\n 14 release indicated that platelets may be a major source of circulating\n TNFSF<\/jats:styled-content>\n 14 in\n SCA<\/jats:styled-content>\n . Interestingly, high plasma\n TNFSF<\/jats:styled-content>\n 14 was significantly associated with elevated tricuspid regurgitant velocity (\u22652\u00b75\u00a0m\/s) in a population of\n SCA<\/jats:styled-content>\n \/\n SCAHC<\/jats:styled-content>\n patients. The pro\u2010inflammatory and atherogenic cytokine,\n TNFSF<\/jats:styled-content>\n 14, could contribute to endothelial activation and inflammation in\n SCA<\/jats:styled-content>\n ; 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.\n <\/jats:p>","DOI":"10.1111\/j.1365-2141.2012.09218.x","type":"journal-article","created":{"date-parts":[[2012,7,6]],"date-time":"2012-07-06T08:34:09Z","timestamp":1341563649000},"page":"788-797","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Elevated plasma levels and platelet\u2010associated expression of the pro\u2010thrombotic and pro\u2010inflammatory protein,\n T<\/scp>\n NFSF14 (LIGHT), in sickle cell disease"],"prefix":"10.1111","volume":"158","author":[{"given":"Vanessa T.","family":"Garrido","sequence":"first","affiliation":[{"name":"INCT de Sangue, Haematology and Haemotherapy Centre School of Medicine University of Campinas \u2013UNICAMP Campinas SP Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renata","family":"Proen\u00e7a\u2010Ferreira","sequence":"additional","affiliation":[{"name":"INCT de Sangue, Haematology and Haemotherapy Centre School of Medicine University of Campinas \u2013UNICAMP Campinas SP Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Venina M.","family":"Dominical","sequence":"additional","affiliation":[{"name":"INCT de Sangue, Haematology and Haemotherapy Centre School of Medicine University of Campinas \u2013UNICAMP Campinas SP Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabiola","family":"Traina","sequence":"additional","affiliation":[{"name":"INCT de Sangue, Haematology and Haemotherapy Centre School of Medicine University of Campinas \u2013UNICAMP Campinas SP Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcos A. C.","family":"Bezerra","sequence":"additional","affiliation":[{"name":"Centro de Ci\u00eancias Biol\u00f3gicas Universidade Federal de Pernambuco Recife PE PE Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariana R. B.","family":"de Mello","sequence":"additional","affiliation":[{"name":"INCT de Sangue, Haematology and Haemotherapy Centre School of Medicine University of Campinas \u2013UNICAMP Campinas SP Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marina P.","family":"Colella","sequence":"additional","affiliation":[{"name":"INCT de Sangue, Haematology and Haemotherapy Centre School of Medicine University of Campinas \u2013UNICAMP Campinas SP Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aderson S.","family":"Ara\u00fajo","sequence":"additional","affiliation":[{"name":"Haematology and Haemotherapy Foundation of Pernambuco (HEMOPE) Recife PE Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sara T. 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