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A rat model of human FENIB (familial encephalopathy with neuroserpin inclusion bodies).

Abstract：

:FENIB (familial encephalopathy with neuroserpin inclusion bodies) is caused by intracellular accumulation/polymerization of mutant neuroserpins in the endoplasmic reticulum (ER). Transgenic rats overexpressing megsin (Tg meg), a newly identified serine protease inhibitor (serpin), demonstrated intraneuronal periodic-acid Schiff (PAS)-positive inclusions distributed throughout deeper layers of cerebral cortex, CA1 of the hippocampus, and substantia nigra. Hippocampal extracts from Tg meg rats showed increased expression of ER stress proteins, and activation of caspases-12 and -3, associated with decreased neuronal density. Enhanced ER stress was also observed in dopaminergic neurons in the substantia nigra, in parallel with decreased neuronal viability and motor coordination. In each case, PAS-positive inclusions were also positive for megsin. These data suggest that overexpression of megsin results in ER stress, eventuating in the formation of PAS-positive inclusions. Tg meg rats provide a novel model of FENIB, where accumulation of serpins in the ER induces selective dysfunction/loss of specific neuronal populations.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Takano K,Kitao Y,Inagi R,Momoi T,Matsuyama T,Miyata T,Yoneda Y,Iso H,Stern DM,Hori O,Ogawa S

doi

10.1016/j.bbrc.2006.06.016

subject

Has Abstract

pub_date

2006-08-04 00:00:00

pages

1040-7

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(06)01302-7

journal_volume

346

pub_type

杂志文章

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