Research ArticlePhysiology

Lipid-Induced Toxicity Stimulates Hepatocytes to Release Angiogenic Microparticles That Require Vanin-1 for Uptake by Endothelial Cells

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Science Signaling  08 Oct 2013:
Vol. 6, Issue 296, pp. ra88
DOI: 10.1126/scisignal.2004512

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Sending an Angiogenic Message

Excess amounts of saturated fatty acids are a potential dietary trigger for the fatty liver disease steatohepatitis, in which the liver develops fat deposits and inflammation. Progression of the disease to more serious forms, which can include scarring and other serious complications, is associated with the formation of new blood vessels, a process called angiogenesis, which requires endothelial cells to migrate and form tubular structures. Povero et al. found that a hepatocyte cell line exposed to excess amounts of saturated fatty acids released membrane-bound microparticles that induced angiogenesis when administered to mice. Microparticles from the blood of mice with diet-induced steatohepatitis originated from the liver and triggered migration and tubular structure formation when applied to an endothelial cell line. The angiogenic effects of microparticles generated by a hepatocyte cell line exposed to saturated fatty acids or of those from mice with diet-induced steatohepatitis involved the uptake of the microparticles by endothelial cells, a process that required Vanin-1, an enzyme located on the surface of the microparticles. Thus, the pathological angiogenesis that can occur in steatohepatitis could be reduced by preventing endothelial cells from internalizing Vanin-1–positive microparticles from hepatocytes.

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