APP mRNA splicing is upregulated in the brain of biglycan transgenic mice

Annamária Bjelik, M. Pákáski, Erika Bereczki, Szilvia Gonda, A. Juhász, A. Rimanóczy, Marianna Zana, Z. Janka, M. Sántha, J. Kálmán

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Many of the risk factors for cerebrovascular disease and atherosclerosis also increase the risk of Alzheimer's disease, characterized by the cerebral deposition of β-amyloid plaques resulting from the abnormal processing of the transmembrane amyloid precursor protein (APP). The initiating event of cholesterol-induced atherosclerosis is the retention and accumulation of atherogenic apolipoprotein B (apoB) together with low-density lipoproteins in the vascular intima. Biglycan, a member of the small leucine-rich protein family, was suspected of contributing to this process. The individual and combined overexpressions of biglycan and apoB-100 were therefore examined on the cortical APP mRNA levels of transgenic mice by means of semiquantitative PCR. As compared with the control littermates, transgenic biglycan mice had significantly increased cortical APP695 (122%) and APP770 (157%) mRNA levels, while the double transgenic (apoB+/- × biglycan+/-) mice did not exhibit any changes. These results provide the first experimental evidence that the atherogenic risk factor biglycan alters APP splicing and may participate in the pathogenesis of both Alzheimer and vascular dementias.

Original languageEnglish
Pages (from-to)1-4
Number of pages4
JournalNeurochemistry International
Volume50
Issue number1
DOIs
Publication statusPublished - Jan 2007

Fingerprint

Biglycan
Protein Splicing
Amyloid
Transgenic Mice
Messenger RNA
Brain
Amyloid beta-Protein Precursor
Atherosclerosis
Alzheimer Disease
Tunica Intima
Apolipoprotein B-100
Cerebrovascular Disorders
Vascular Dementia
Amyloid Plaques
Apolipoproteins B
LDL Lipoproteins
Leucine
Cholesterol
Polymerase Chain Reaction
Proteins

Keywords

  • Alzheimer's disease
  • Amyloid precursor protein
  • apoB
  • Atherosclerosis
  • Biglycan
  • Transgenic mice
  • Vascular

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Cellular and Molecular Neuroscience

Cite this

APP mRNA splicing is upregulated in the brain of biglycan transgenic mice. / Bjelik, Annamária; Pákáski, M.; Bereczki, Erika; Gonda, Szilvia; Juhász, A.; Rimanóczy, A.; Zana, Marianna; Janka, Z.; Sántha, M.; Kálmán, J.

In: Neurochemistry International, Vol. 50, No. 1, 01.2007, p. 1-4.

Research output: Contribution to journalArticle

@article{526186b572eb426aa9bd2e2ac1606ea5,
title = "APP mRNA splicing is upregulated in the brain of biglycan transgenic mice",
abstract = "Many of the risk factors for cerebrovascular disease and atherosclerosis also increase the risk of Alzheimer's disease, characterized by the cerebral deposition of β-amyloid plaques resulting from the abnormal processing of the transmembrane amyloid precursor protein (APP). The initiating event of cholesterol-induced atherosclerosis is the retention and accumulation of atherogenic apolipoprotein B (apoB) together with low-density lipoproteins in the vascular intima. Biglycan, a member of the small leucine-rich protein family, was suspected of contributing to this process. The individual and combined overexpressions of biglycan and apoB-100 were therefore examined on the cortical APP mRNA levels of transgenic mice by means of semiquantitative PCR. As compared with the control littermates, transgenic biglycan mice had significantly increased cortical APP695 (122{\%}) and APP770 (157{\%}) mRNA levels, while the double transgenic (apoB+/- × biglycan+/-) mice did not exhibit any changes. These results provide the first experimental evidence that the atherogenic risk factor biglycan alters APP splicing and may participate in the pathogenesis of both Alzheimer and vascular dementias.",
keywords = "Alzheimer's disease, Amyloid precursor protein, apoB, Atherosclerosis, Biglycan, Transgenic mice, Vascular",
author = "Annam{\'a}ria Bjelik and M. P{\'a}k{\'a}ski and Erika Bereczki and Szilvia Gonda and A. Juh{\'a}sz and A. Riman{\'o}czy and Marianna Zana and Z. Janka and M. S{\'a}ntha and J. K{\'a}lm{\'a}n",
year = "2007",
month = "1",
doi = "10.1016/j.neuint.2006.07.009",
language = "English",
volume = "50",
pages = "1--4",
journal = "Neurochemistry International",
issn = "0197-0186",
publisher = "Elsevier Limited",
number = "1",

}

TY - JOUR

T1 - APP mRNA splicing is upregulated in the brain of biglycan transgenic mice

AU - Bjelik, Annamária

AU - Pákáski, M.

AU - Bereczki, Erika

AU - Gonda, Szilvia

AU - Juhász, A.

AU - Rimanóczy, A.

AU - Zana, Marianna

AU - Janka, Z.

AU - Sántha, M.

AU - Kálmán, J.

PY - 2007/1

Y1 - 2007/1

N2 - Many of the risk factors for cerebrovascular disease and atherosclerosis also increase the risk of Alzheimer's disease, characterized by the cerebral deposition of β-amyloid plaques resulting from the abnormal processing of the transmembrane amyloid precursor protein (APP). The initiating event of cholesterol-induced atherosclerosis is the retention and accumulation of atherogenic apolipoprotein B (apoB) together with low-density lipoproteins in the vascular intima. Biglycan, a member of the small leucine-rich protein family, was suspected of contributing to this process. The individual and combined overexpressions of biglycan and apoB-100 were therefore examined on the cortical APP mRNA levels of transgenic mice by means of semiquantitative PCR. As compared with the control littermates, transgenic biglycan mice had significantly increased cortical APP695 (122%) and APP770 (157%) mRNA levels, while the double transgenic (apoB+/- × biglycan+/-) mice did not exhibit any changes. These results provide the first experimental evidence that the atherogenic risk factor biglycan alters APP splicing and may participate in the pathogenesis of both Alzheimer and vascular dementias.

AB - Many of the risk factors for cerebrovascular disease and atherosclerosis also increase the risk of Alzheimer's disease, characterized by the cerebral deposition of β-amyloid plaques resulting from the abnormal processing of the transmembrane amyloid precursor protein (APP). The initiating event of cholesterol-induced atherosclerosis is the retention and accumulation of atherogenic apolipoprotein B (apoB) together with low-density lipoproteins in the vascular intima. Biglycan, a member of the small leucine-rich protein family, was suspected of contributing to this process. The individual and combined overexpressions of biglycan and apoB-100 were therefore examined on the cortical APP mRNA levels of transgenic mice by means of semiquantitative PCR. As compared with the control littermates, transgenic biglycan mice had significantly increased cortical APP695 (122%) and APP770 (157%) mRNA levels, while the double transgenic (apoB+/- × biglycan+/-) mice did not exhibit any changes. These results provide the first experimental evidence that the atherogenic risk factor biglycan alters APP splicing and may participate in the pathogenesis of both Alzheimer and vascular dementias.

KW - Alzheimer's disease

KW - Amyloid precursor protein

KW - apoB

KW - Atherosclerosis

KW - Biglycan

KW - Transgenic mice

KW - Vascular

UR - http://www.scopus.com/inward/record.url?scp=33845300510&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33845300510&partnerID=8YFLogxK

U2 - 10.1016/j.neuint.2006.07.009

DO - 10.1016/j.neuint.2006.07.009

M3 - Article

C2 - 16962684

AN - SCOPUS:33845300510

VL - 50

SP - 1

EP - 4

JO - Neurochemistry International

JF - Neurochemistry International

SN - 0197-0186

IS - 1

ER -