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Journal of Lipid Research
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    • Research Article3

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    • Research Article
      Open Access

      Atherosclerosis-associated hepatic secretion of VLDL but not PCSK9 is dependent on cargo receptor protein Surf4

      Journal of Lipid Research
      Vol. 62100091Published online: June 9, 2021
      • Bingxiang Wang
      • Yishi Shen
      • Lei Zhai
      • Xiaodan Xia
      • Hong-mei Gu
      • Maggie Wang
      • and others
      Cited in Scopus: 0
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        Plasma LDL is produced from catabolism of VLDL and cleared from circulation mainly via the hepatic LDL receptor (LDLR). Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes LDLR degradation, increasing plasma LDL-C levels. Circulating PCSK9 is mainly secreted by the liver, whereas VLDL is exclusively secreted by hepatocytes. However, the mechanism regulating their secretion is not completely understood. Surfeit 4 (Surf4) is a cargo receptor localized in the ER membrane. It recruits cargos into coat protein complex II vesicles to facilitate their secretion.
        Atherosclerosis-associated hepatic secretion of VLDL but not PCSK9 is dependent on cargo receptor protein Surf4
      • Research Article
        Open Access

        Nonalcoholic fatty liver disease stratification by liver lipidomics

        Journal of Lipid Research
        Vol. 62100104Published online: August 9, 2021
        • Olga Vvedenskaya
        • Tim Daniel Rose
        • Oskar Knittelfelder
        • Alessandra Palladini
        • Judith Andrea Heidrun Wodke
        • Kai Schuhmann
        • and others
        Cited in Scopus: 18
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          Nonalcoholic fatty liver disease (NAFLD) is a common metabolic dysfunction leading to hepatic steatosis. However, NAFLD's global impact on the liver lipidome is poorly understood. Using high-resolution shotgun mass spectrometry, we quantified the molar abundance of 316 species from 22 major lipid classes in liver biopsies of 365 patients, including nonsteatotic patients with normal or excessive weight, patients diagnosed with NAFL (nonalcoholic fatty liver) or NASH (nonalcoholic steatohepatitis), and patients bearing common mutations of NAFLD-related protein factors.
          Nonalcoholic fatty liver disease stratification by liver lipidomics
        • Research Article
          Open Access

          Human cholesteryl ester transfer protein lacks lipopolysaccharide transfer activity, but worsens inflammation and sepsis outcomes in mice

          Journal of Lipid Research
          Vol. 62100011Published online: December 15, 2020
          • Aloïs Dusuel
          • Valérie Deckert
          • Jean-Paul Pais de Barros
          • Kevin van Dongen
          • Hélène Choubley
          • Émilie Charron
          • and others
          Cited in Scopus: 0
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            Bacterial lipopolysaccharides (LPSs or endotoxins) can bind most proteins of the lipid transfer/LPS-binding protein (LT/LBP) family in host organisms. The LPS-bound LT/LBP proteins then trigger either an LPS-induced proinflammatory cascade or LPS binding to lipoproteins that are involved in endotoxin inactivation and detoxification. Cholesteryl ester transfer protein (CETP) is an LT/LBP member, but its impact on LPS metabolism and sepsis outcome is unclear. Here, we performed fluorescent LPS transfer assays to assess the ability of CETP to bind and transfer LPS.
            Human cholesteryl ester transfer protein lacks lipopolysaccharide transfer activity, but worsens inflammation and sepsis outcomes in mice
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