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Title: Proteomic profiling of brain cortex tissues in a Tau transgenic mouse model of Alzheimer's disease

Abstract

Highlights: Black-Right-Pointing-Pointer A transgenic mouse model expressing NSE-htau23 was used. Black-Right-Pointing-Pointer 2D-gel electrophoresis to analyze the cortex proteins of transgenic mice was used. Black-Right-Pointing-Pointer Differentially expressed spots in different stages of AD were identified. Black-Right-Pointing-Pointer GSTP1 and CAII were downregulated with the progression of AD. Black-Right-Pointing-Pointer SCRN1 and ATP6VE1 were up regulated and down regulated differentially. -- Abstract: Alzheimer's disease (AD) involves regionalized neuronal death, synaptic loss, and an accumulation of intracellular neurofibrillary tangles and extracellular senile plaques. Although there have been numerous studies on tau proteins and AD in various stages of neurodegenerative disease pathology, the relationship between tau and AD is not yet fully understood. A transgenic mouse model expressing neuron-specific enolase (NSE)-controlled human wild-type tau (NSE-htau23), which displays some of the typical Alzheimer-associated pathological features, was used to analyze the brain proteome associated with tau tangle deposition. Two-dimensional electrophoresis was performed to compare the cortex proteins of transgenic mice (6- and 12-month-old) with those of control mice. Differentially expressed spots in different stages of AD were identified with ESI-Q-TOF (electrospray ionization quadruple time-of-flight) mass spectrometry and liquid chromatography/tandem mass spectrometry. Among the identified proteins, glutathione S-transferase P 1 (GSTP1) and carbonic anhydrase II (CAII) were down-regulated withmore » the progression of AD, and secerin-1 (SCRN1) and V-type proton ATPase subunit E 1 (ATP6VE1) were up-regulated only in the early stages, and down-regulated in the later stages of AD. The proteins, which were further confirmed by RT-PCR at the mRNA level and with western blotting at the protein level, are expected to be good candidates as drug targets for AD. The study of up- and down-regulation of proteins during the progression of AD helps to explain the mechanisms associated with neuronal degeneration in AD.« less

Authors:
; ; ; ;  [1];  [1]
  1. School of Life Sciences and Biotechnology, Korea University, Seoul 136-701 (Korea, Republic of)
Publication Date:
OSTI Identifier:
22210384
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 430; Journal Issue: 2; Other Information: Copyright (c) 2012 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANIMAL TISSUES; BRAIN; CARBONIC ANHYDRASE; CEREBROSPINAL FLUID; GLUTATHIONE; LIQUID COLUMN CHROMATOGRAPHY; MASS SPECTROSCOPY; MESSENGER-RNA; NERVE CELLS; NERVOUS SYSTEM DISEASES; NEUTRON SPECTROSCOPY; NUCLEOSIDES; PATHOLOGY; PHOSPHATES; POLYMERASE CHAIN REACTION; SPIN ECHO; TIME-OF-FLIGHT METHOD; TRANSGENIC MICE

Citation Formats

Chang, Seong-Hun, Jung, In-Soo, Han, Gi-Yeon, Kim, Nam-Hee, Kim, Hyun-Jung, and Kim, Chan-Wha. Proteomic profiling of brain cortex tissues in a Tau transgenic mouse model of Alzheimer's disease. United States: N. p., 2013. Web. doi:10.1016/J.BBRC.2012.11.093.
Chang, Seong-Hun, Jung, In-Soo, Han, Gi-Yeon, Kim, Nam-Hee, Kim, Hyun-Jung, & Kim, Chan-Wha. Proteomic profiling of brain cortex tissues in a Tau transgenic mouse model of Alzheimer's disease. United States. https://doi.org/10.1016/J.BBRC.2012.11.093
Chang, Seong-Hun, Jung, In-Soo, Han, Gi-Yeon, Kim, Nam-Hee, Kim, Hyun-Jung, and Kim, Chan-Wha. 2013. "Proteomic profiling of brain cortex tissues in a Tau transgenic mouse model of Alzheimer's disease". United States. https://doi.org/10.1016/J.BBRC.2012.11.093.
@article{osti_22210384,
title = {Proteomic profiling of brain cortex tissues in a Tau transgenic mouse model of Alzheimer's disease},
author = {Chang, Seong-Hun and Jung, In-Soo and Han, Gi-Yeon and Kim, Nam-Hee and Kim, Hyun-Jung and Kim, Chan-Wha},
abstractNote = {Highlights: Black-Right-Pointing-Pointer A transgenic mouse model expressing NSE-htau23 was used. Black-Right-Pointing-Pointer 2D-gel electrophoresis to analyze the cortex proteins of transgenic mice was used. Black-Right-Pointing-Pointer Differentially expressed spots in different stages of AD were identified. Black-Right-Pointing-Pointer GSTP1 and CAII were downregulated with the progression of AD. Black-Right-Pointing-Pointer SCRN1 and ATP6VE1 were up regulated and down regulated differentially. -- Abstract: Alzheimer's disease (AD) involves regionalized neuronal death, synaptic loss, and an accumulation of intracellular neurofibrillary tangles and extracellular senile plaques. Although there have been numerous studies on tau proteins and AD in various stages of neurodegenerative disease pathology, the relationship between tau and AD is not yet fully understood. A transgenic mouse model expressing neuron-specific enolase (NSE)-controlled human wild-type tau (NSE-htau23), which displays some of the typical Alzheimer-associated pathological features, was used to analyze the brain proteome associated with tau tangle deposition. Two-dimensional electrophoresis was performed to compare the cortex proteins of transgenic mice (6- and 12-month-old) with those of control mice. Differentially expressed spots in different stages of AD were identified with ESI-Q-TOF (electrospray ionization quadruple time-of-flight) mass spectrometry and liquid chromatography/tandem mass spectrometry. Among the identified proteins, glutathione S-transferase P 1 (GSTP1) and carbonic anhydrase II (CAII) were down-regulated with the progression of AD, and secerin-1 (SCRN1) and V-type proton ATPase subunit E 1 (ATP6VE1) were up-regulated only in the early stages, and down-regulated in the later stages of AD. The proteins, which were further confirmed by RT-PCR at the mRNA level and with western blotting at the protein level, are expected to be good candidates as drug targets for AD. The study of up- and down-regulation of proteins during the progression of AD helps to explain the mechanisms associated with neuronal degeneration in AD.},
doi = {10.1016/J.BBRC.2012.11.093},
url = {https://www.osti.gov/biblio/22210384}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 430,
place = {United States},
year = {Fri Jan 11 00:00:00 EST 2013},
month = {Fri Jan 11 00:00:00 EST 2013}
}