Lipopolysaccharide-binding protein (LBP) reverses the amyloid state of fibrin seen in plasma of type 2 diabetics with cardiovascular comorbidities

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dc.contributor.authorPretorius, Etheresiaen_ZA
dc.contributor.authorMbotwe, Sthembileen_ZA
dc.contributor.authorKell, Douglas B.en_ZA
dc.date.accessioned2018-11-30T10:15:33Z
dc.date.available2018-11-30T10:15:33Z
dc.date.issued2017-08-29
dc.descriptionCITATION: Pretorius, E., Mbotwe, S. & Kell, D. B. 2017. Lipopolysaccharide-binding protein (LBP) reverses the amyloid state of fibrin seen in plasma of type 2 diabetics with cardiovascular comorbidities. Scientific Reports, 7:9680, doi:1038/s41598-017-09860-4.en_ZA
dc.descriptionThe original publication is available at https://www.nature.comen_ZA
dc.description.abstractType 2 diabetes (T2D) has many cardiovascular complications, including a thrombotic propensity. Many such chronic, inflammatory diseases are accompanied (and may be exacerbated, and possibly even largely caused) by amyloid fibril formation. Recognising that there are few strong genetic associations underpinning T2D, but that amyloidogenesis of amylin is closely involved, we have been seeking to understand what might trigger the disease. Serum levels of bacterial lipopolysaccharide are raised in T2D, and we recently showed that fibrin(ogen) polymerisation during blood clotting can be affected strongly by LPS. The selectivity was indicated by the regularisation of clotting by lipopolysaccharide-binding protein (LBP). Since coagulopathies are a hallmark of T2D, we wondered whether they might too be caused by LPS (and reversed by LBP). We show here, using SEM and confocal microscopy, that platelet-poor-plasma from subjects with T2D had a much greater propensity for hypercoagulability and for amyloidogenesis, and that these could both be reversed by LBP. These data imply that coagulopathies are an important feature of T2D, and may be driven by ‘hidden’ LPS. Given the prevalence of amyloid formation in the sequelae of diabetes, this opens up novel strategies for both the prevention and treatment of T2D.en_ZA
dc.description.urihttps://www.nature.com/articles/s41598-017-09860-4
dc.description.versionPublisher's versionen_ZA
dc.format.extent16 pages : illustrationsen_ZA
dc.identifier.citationPretorius, E., Mbotwe, S. & Kell, D. B. 2017. Lipopolysaccharide-binding protein (LBP) reverses the amyloid state of fibrin seen in plasma of type 2 diabetics with cardiovascular comorbidities. Scientific Reports, 7:9680, doi:1038/s41598-017-09860-4en_ZA
dc.identifier.issn2045-2322 (online)
dc.identifier.otherdoi:1038/s41598-017-09860-4
dc.identifier.urihttp://hdl.handle.net/10019.1/104758
dc.language.isoen_ZAen_ZA
dc.publisherNature Researchen_ZA
dc.rights.holderAuthors retain copyrighten_ZA
dc.subjectType 2 diabetesen_ZA
dc.subjectType 2 diabetes (T2D) -- Treatmenten_ZA
dc.subjectType 2 diabetes (T2D) -- Preventionen_ZA
dc.subjectAmyloid fibril formationen_ZA
dc.subjectLipopolysaccharide-binding protein (LBP)en_ZA
dc.titleLipopolysaccharide-binding protein (LBP) reverses the amyloid state of fibrin seen in plasma of type 2 diabetics with cardiovascular comorbiditiesen_ZA
dc.typeArticleen_ZA
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