東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back

Switch To: Labeled | MARC Mode | ISBD

The effects of apolipoprotein E and ...

Chen, Shuang.

Linked to FindBook

Google Book

Amazon

博客來

The effects of apolipoprotein E and beta amyloid protein on secretion of inflammatory mediators in adult rat microglia.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	The effects of apolipoprotein E and beta amyloid protein on secretion of inflammatory mediators in adult rat microglia./
Author:	Chen, Shuang.
Description:	147 p.
Notes:	Adviser: March D. Ard.
Contained By:	Dissertation Abstracts International64-05B.
Subject:	Biology, Neuroscience. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3091786
ISBN:	9780496394951

The effects of apolipoprotein E and beta amyloid protein on secretion of inflammatory mediators in adult rat microglia.
Chen, Shuang.

The effects of apolipoprotein E and beta amyloid protein on secretion of inflammatory mediators in adult rat microglia. - 147 p.

Adviser: March D. Ard.

Thesis (Ph.D.)--The University of Mississippi Medical Center, 2003.

Inflammation has been suggested to contribute to the pathogenesis of Alzheimer's disease (AD). Microglia are the immune cells in the central nervous system, and when activated they secrete the lipid-derived mediator prostaglandin E2 (PGE2), interleukin-1beta (IL-1beta), and other inflammatory mediators. The importance of inflammation in AD is underlined by the efficacy of nonsteroidal anti-inflammatory drugs, which block PGE2 production against progression of AD. The epsilon allele of the gene APOE 4, coding for apolipoprotein E epsilon 4 (apoE4), has been shown to correlate with higher risk and earlier age of onset of AD. Excessive accumulation of amyloid deposits and soluble beta amyloid protein (Abeta) occurs in the brain in AD. This study investigated the effects of apoE and Abeta on the regulation of PGE2 and IL-1beta secretion in primary microglial culture from adult rat brain cortex. PGE2 and IL-1beta were measured by specific enzyme-immunoassay and expression of the PGE2 synthesizing enzyme cyclooxygenase-2 (COX-2) was measured by immunocytochemistry.

ISBN: 9780496394951Subjects--Topical Terms:

1017680
Biology, Neuroscience.

The effects of apolipoprotein E and beta amyloid protein on secretion of inflammatory mediators in adult rat microglia.
LDR:03110nam 2200289 a 45 001 958428
005 20110704
008 110704s2003 eng d
020 $a 9780496394951
035 $a (UMI)AAI3091786
035 $a AAI3091786
040 $a UMI $c UMI
100 1 $a Chen, Shuang. $3 1281889
245 1 4 $a The effects of apolipoprotein E and beta amyloid protein on secretion of inflammatory mediators in adult rat microglia.
300 $a 147 p.
500 $a Adviser: March D. Ard.
500 $a Source: Dissertation Abstracts International, Volume: 64-05, Section: B, page: 2056.
502 $a Thesis (Ph.D.)--The University of Mississippi Medical Center, 2003.
520 $a Inflammation has been suggested to contribute to the pathogenesis of Alzheimer's disease (AD). Microglia are the immune cells in the central nervous system, and when activated they secrete the lipid-derived mediator prostaglandin E2 (PGE2), interleukin-1beta (IL-1beta), and other inflammatory mediators. The importance of inflammation in AD is underlined by the efficacy of nonsteroidal anti-inflammatory drugs, which block PGE2 production against progression of AD. The epsilon allele of the gene APOE 4, coding for apolipoprotein E epsilon 4 (apoE4), has been shown to correlate with higher risk and earlier age of onset of AD. Excessive accumulation of amyloid deposits and soluble beta amyloid protein (Abeta) occurs in the brain in AD. This study investigated the effects of apoE and Abeta on the regulation of PGE2 and IL-1beta secretion in primary microglial culture from adult rat brain cortex. PGE2 and IL-1beta were measured by specific enzyme-immunoassay and expression of the PGE2 synthesizing enzyme cyclooxygenase-2 (COX-2) was measured by immunocytochemistry.
520 $a The primary finding in this study is that apoE4 alone can stimulate rat microglia in culture to secrete PGE2 and IL-1beta in the presence of serum. The increase in PGE2 release was not accompanied by the upregulation of COX-2. Neither Abeta1-40 nor Abeta1-42 alone induced PGE2 and IL-1beta secretion from microglia. In studies using a co-stimulator (LPS), the combination of apoE3 and Abeta1-40 inhibited PGE2 and IL-1beta secretion stimulated by LPS in serum-free medium. Soluble Abeta1-40 alone did not modulate the LPS-induced secretion of PGE2 in medium with serum, whereas soluble Abeta1-42 attenuated LPS-induced secretion of PGE2 and COX-2 expression. Fibrillar Abeta1-40 or Abeta1-42 themselves did not increase the secretion of PGE2 or modulate LPS induced PGE2 secretion.
520 $a In conclusion, apoE4, but not the more common apoE3, activates microglia to secrete the inflammatory mediators PGE2 and IL-1beta. This is the first demonstration of a direct inflammatory activity of apoE4. Surprisingly, the Abeta proteins had only minor modulatory effects of microglia in this study.
590 $a School code: 0805.
650 4 $a Biology, Neuroscience. $3 1017680
690 $a 0317
710 2 0 $a The University of Mississippi Medical Center. $3 1017852
773 0 $t Dissertation Abstracts International $g 64-05B.
790 $a 0805
790 1 0 $a Ard, March D., $e advisor
791 $a Ph.D.
792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3091786