Apolipoprotein E-mediated regulation of selenoprotein P transportation via exosomes

Yunjung Jin, Youn Wook Chung, Min Kyo Jung, Jea Hwang Lee, Kwan Young Ko, Jun Ki Jang, Minju Ham, Hyunwoo Kang, Chan Gi Pack, Hisaaki Mihara, Ick Young Kim

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


Selenoprotein P (SELENOP), secreted from the liver, functions as a selenium (Se) supplier to other tissues. In the brain, Se homeostasis is critical for physiological function. Previous studies have reported that SELENOP co-localizes with the apolipoprotein E receptor 2 (ApoER2) along the blood–brain barrier (BBB). However, the mechanism underlying SELENOP transportation from hepatocytes to neuronal cells remains unclear. Here, we found that SELENOP was secreted from hepatocytes as an exosomal component protected from plasma kallikrein-mediated cleavage. SELENOP was interacted with apolipoprotein E (ApoE) through heparin-binding sites of SELENOP, and the interaction regulated the secretion of exosomal SELENOP. Using in vitro BBB model of transwell cell culture, exosomal SELENOP was found to supply Se to brain endothelial cells and neuronal cells, which synthesized selenoproteins by a process regulated by ApoE and ApoER2. The regulatory role of ApoE in SELENOP transport was also observed in vivo using ApoE−/− mice. Exosomal SELENOP transport protected neuronal cells from amyloid β (Aβ)-induced cell death. Taken together, our results suggest a new delivery mechanism for Se to neuronal cells by exosomal SELENOP.

Original languageEnglish
Pages (from-to)2367-2386
Number of pages20
JournalCellular and Molecular Life Sciences
Issue number12
Publication statusPublished - 2020 Jun 1


  • Amyloid β
  • Apolipoprotein E
  • Exosome
  • Protein transport
  • Selenoprotein P

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Pharmacology
  • Cellular and Molecular Neuroscience
  • Cell Biology


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