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- Gautam, Narinder, et al.
(author)
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Heparin-binding protein (HBP/CAP37): A missing link in neutrophil-evoked alteration of vascular permeability
- 2001
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In: Nature Medicine. - : Springer Science and Business Media LLC. - 1546-170X .- 1078-8956. ; 7:10, s. 1123-1127
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Journal article (peer-reviewed)abstract
- Polymorphonuclear leukocyte infiltration into tissues in host defense and inflammatory diseasecauses increased vascular permeability and edema formation through unknown mechanisms.Here, we report the involvement of a paracrine mechanism in neutrophil-evoked alteration inendothelial barrier function. We show that upon neutrophil adhesion to the endothelial lining,leukocytic 2 integrin signaling triggers the release of neutrophil-borne heparin-binding protein(HBP), also known as CAP37/azurocidin, a member of the serprocidin family of neutrophilcationic proteins. HBP induced Ca++-dependent cytoskeletal rearrangement and intercellular gapformation in endothelial-cell monolayers in vitro, and increased macromolecular efflux in microvesselsin vivo. Moreover, selective inactivation of HBP prevented the neutrophils from inducingendothelial hyperpermeability. Our data suggest a fundamental role of neutrophil-derivedHBP in the vascular response to neutrophil trafficking in inflammation. Targeting this moleculein inflammatory disease conditions offers a new strategy for prevention of endothelial barrierdysfunction caused by misdirected leukocyte activation.
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- Scherstén, Tore, 1930, et al.
(author)
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The cholesterol hypothesis: time for the obituary?
- 2011
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In: Scandinavian cardiovascular journal : SCJ. - : Informa UK Limited. - 1651-2006 .- 1401-7431. ; 45:6, s. 322-3
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Journal article (peer-reviewed)abstract
- The cholesterol hypothesis links cholesterol intake and blood levels to cardiovascular disease. It has had enormous impact on health care and society during decades, but has little or no scientific backing that is relevant for the human species. Apparently, the hypothesis is false and should be buried.
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