Secretin receptor involvement in prion-infected cells and animals

FEBS Lett. 2015 Jul 8;589(15):2011-8. doi: 10.1016/j.febslet.2015.05.039. Epub 2015 May 30.

Abstract

The cellular mechanisms behind prion biosynthesis and metabolism remain unclear. Here we show that secretin signaling via the secretin receptor regulates abnormal prion protein formation in prion-infected cells. Animal studies demonstrate that secretin receptor deficiency slightly, but significantly, prolongs incubation time in female but not male mice. This gender-specificity is consistent with our finding that prion-infected cells are derived from females. Therefore, our results provide initial insights into the reasons why age of disease onset in certain prion diseases is reported to occur slightly earlier in females than males.

Keywords: Gender effect; Incubation time; Knockout mouse; N2a cells; Prion; Secretin receptor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Cell Line, Tumor
  • DNA Primers
  • Female
  • Gene Silencing
  • Male
  • Mice
  • Polymerase Chain Reaction
  • Prion Diseases / physiopathology*
  • Receptors, G-Protein-Coupled / genetics
  • Receptors, G-Protein-Coupled / physiology*
  • Receptors, Gastrointestinal Hormone / genetics
  • Receptors, Gastrointestinal Hormone / physiology*
  • Sex Factors

Substances

  • DNA Primers
  • Receptors, G-Protein-Coupled
  • Receptors, Gastrointestinal Hormone
  • secretin receptor