on March 20, 2003
Published online before print March 20, 2003, doi: 10.1161/01.STR.0000064320.73388.C6
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on November 11, 2002
From the Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience (K.A., T.U., N.S., A.N.), Tokyo; Department of Neurology, Fujigaoka Hospital of Showa University (K.A., Y.W.), Yokohama; Department of Neurology, Saitama Rehabilitation Center (N.S.), Saitama; Department of Neuropathology, Tokyo Institute of Psychiatry (K.I., K.T.), Tokyo; and Department of Laboratory Medicine and Pathology, Tokyo Metropolitan Matsuzawa Hospital (K.T.), Tokyo, Japan. * To whom correspondence should be addressed. E-mail: uchihara{at}tmin.ac.jp.
Background and Purpose--Cellular origin of apolipoprotein E (ApoE) in the human brain and its roles in physiological and pathological conditions remain to be clarified. Methods--Immunolocalization of ApoE was investigated in a series of autopsied human brains with or without infarction. ApoE expression was also estimated on immunoblot on protein extracts from autopsied brains and a cultured neuroblastoma cell line of human origin (GOTO) subjected to an oxidative stress induced by exposure to hydrogen peroxide (0.2 mmol/L). Results--In addition to astrocytes and microglia, neurons and degenerated axons in and around the ischemic foci contained ApoE-like immunoreactivity, which was more intense in recent ischemic foci. Immunoblot demonstrated an increase in expression of ApoE in brain extracts from ischemic lesion, and this increase was also pronounced in the cultured neuroblastoma cell line after the stress. Conclusions--Accumulation of ApoE in neurons in and around ischemic foci of the human brain is related to an increase in ApoE synthesis in neurons, as seen in cultured neuronal cells after oxidative stress. Intrinsic regenerative activity of neuron in reaction to external insults may be related to this increase in ApoE of neuronal origin.
Accepted on November 13, 2002
Increased Expression of Neuronal Apolipoprotein E in Human Brain With Cerebral Infarction
Kazuko Aoki MD, PhD;
Key words: apolipoproteins • cerebral infarction • neurons • oxidative stress
This article has been cited by other articles:
 |
|
 |
|
  R. Lu, J. Ito, N. Iwamoto, T. Nishimaki-Mogami, and S. Yokoyama FGF-1 induces expression of LXR{alpha} and production of 25-hydroxycholesterol to upregulate the apoE gene in rat astrocytes J. Lipid Res., June 1, 2009; 50(6): 1156 - 1164. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Nagayasu, J.-i. Ito, T. Nishida, and S. Yokoyama Reactivity of Astrocytes to Fibroblast Growth Factor-1 for Biogenesis of Apolipoprotein E-High Density Lipoprotein is Down-regulated by Long-time Secondary Culture J. Biochem., May 1, 2008; 143(5): 611 - 616. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-i. Ito, Y. Nagayasu, K. Okumura-Noji, R. Lu, T. Nishida, Y. Miura, K. Asai, A. Kheirollah, S. Nakaya, and S. Yokoyama Mechanism for FGF-1 to regulate biogenesis of apoE-HDL in astrocytes J. Lipid Res., September 1, 2007; 48(9): 2020 - 2027. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Q. Xu, A. Bernardo, D. Walker, T. Kanegawa, R. W. Mahley, and Y. Huang Profile and Regulation of Apolipoprotein E (ApoE) Expression in the CNS in Mice with Targeting of Green Fluorescent Protein Gene to the ApoE Locus. J. Neurosci., May 10, 2006; 26(19): 4985 - 4994. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. W. Mahley, K. H. Weisgraber, and Y. Huang Inaugural Article: Apolipoprotein E4: A causative factor and therapeutic target in neuropathology, including Alzheimer's disease PNAS, April 11, 2006; 103(15): 5644 - 5651. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Huang Apolipoprotein E and Alzheimer disease Neurology, January 24, 2006; 66(1_suppl_1): S79 - S85. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Chang, T. r. Ma, R. D. Miranda, M. E. Balestra, R. W. Mahley, and Y. Huang Lipid- and receptor-binding regions of apolipoprotein E4 fragments act in concert to cause mitochondrial dysfunction and neurotoxicity PNAS, December 20, 2005; 102(51): 18694 - 18699. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-i. Ito, Y. Nagayasu, R. Lu, A. Kheirollah, M. Hayashi, and S. Yokoyama Astrocytes produce and secrete FGF-1, which promotes the production of apoE-HDL in a manner of autocrine action J. Lipid Res., April 1, 2005; 46(4): 679 - 686. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Q. Xu, W. J. Brecht, K. H. Weisgraber, R. W. Mahley, and Y. Huang Apolipoprotein E4 Domain Interaction Occurs in Living Neuronal Cells as Determined by Fluorescence Resonance Energy Transfer J. Biol. Chem., June 11, 2004; 279(24): 25511 - 25516. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. J. Brecht, F. M. Harris, S. Chang, I. Tesseur, G.-Q. Yu, Q. Xu, J. Dee Fish, T. Wyss-Coray, M. Buttini, L. Mucke, et al. Neuron-Specific Apolipoprotein E4 Proteolysis Is Associated with Increased Tau Phosphorylation in Brains of Transgenic Mice J. Neurosci., March 10, 2004; 24(10): 2527 - 2534. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. M. Harris, I. Tesseur, W. J. Brecht, Q. Xu, K. Mullendorff, S. Chang, T. Wyss-Coray, R. W. Mahley, and Y. Huang Astroglial Regulation of Apolipoprotein E Expression in Neuronal Cells: IMPLICATIONS FOR ALZHEIMER'S DISEASE J. Biol. Chem., January 30, 2004; 279(5): 3862 - 3868. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. M. Harris, W. J. Brecht, Q. Xu, I. Tesseur, L. Kekonius, T. Wyss-Coray, J. D. Fish, E. Masliah, P. C. Hopkins, K. Scearce-Levie, et al. Carboxyl-terminal-truncated apolipoprotein E4 causes Alzheimer's disease-like neurodegeneration and behavioral deficits in transgenic mice PNAS, September 16, 2003; 100(19): 10966 - 10971. [Abstract] [Full Text] [PDF]
|
|