Anoxia leads to a rapid translocation of human trypsinogen 4 to the plasma membrane of cultured astrocytes

Krisztián Tárnok, László Szilágyi, Tímea Berki, Péter Németh, László Gráf, Katalin Schlett

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Abstract

Trypsinogen 4 is specifically expressed in the human brain, mainly by astroglial cells. Although its exact role in the nervous tissue is yet unclear, trypsin 4-mediated pathological processes were suggested in Alzheimer's disease, multiple sclerosis and ischemic injury. In the present study, we analyzed the intracellular distribution of fluorescently tagged human trypsinogen 4 isoforms during normal and anoxic conditions in transfected mouse primary astrocytes. Our results show that initiation of anoxic milieu by the combined action of KCN treatment and glucose deprivation rapidly leads to the association of leader peptide containing trypsinogen 4 constructs to the plasma membrane. Using rhodamine 110 bis-(CBZ-L-isoleucyl-L-prolyl-L-arginine amide), a synthetic chromogen peptide substrate of trypsin, we show that anoxia can promote extracellular activation of trypsinogen 4 indicating that extracellular activation of human trypsinogen 4 can be an important component in neuropathological changes of the injured human brain.

Original languageEnglish
Pages (from-to)314-324
Number of pages11
JournalJournal of neurochemistry
Volume115
Issue number2
DOIs
Publication statusPublished - Oct 1 2010

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Keywords

  • Anoxia
  • Astroglia
  • BZiPAR
  • Brain trypsin
  • Human trypsinogen 4

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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