Prion protein (PrP) is not involved in the pathogenesis of spongiform encephalopathy in transgenic mice expressing interleukin-6 in the brain.
Transgenic mice expressing interleukin-6 (IL6) in the brain exhibit gliosis, spongiosis and neuronal loss. Based on previous findings, we hypothesized that IL6 could upregulate the prion protein (PrP) gene in the central nervous system (CNS) of these mice. Western and Northern blot analysis showed that PrP protein and mRNA levels were comparable to control levels. Furthermore, ultrastructural characterization revealed that spongiosis was actually located in astrocytes. These results indicate that IL6 does not upregulate the cerebral PrP expression in this animal model and that profound astrocytic alterations precipitate the neuronal degeneration observed.
Castelnau
P A
PA
Department of Pathology, University of California at San Diego and the Veterans Affairs Research Service, La Jolla 92093-0612, USA. pcastelnau@ucsd.edu
Campbell
I L
IL
Powell
H C
HC
D000818:Animals; D001921:Brain / Q000378:metabolism*; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D015151:Immunoblotting; D015850:Interleukin-6 / Q000096:biosynthesis*; D051379:Mice; D008822:Mice, Transgenic; D008854:Microscopy, Electron; D017096:Prion Diseases / Q000209:etiology / Q000503:physiopathology*; D011328:Prions / Q000502:physiology*
D005904:Glial Fibrillary Acidic Protein; D015850:Interleukin-6; D011328:Prions