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The role of the small heat shock pro...

Wang, Gang.

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The role of the small heat shock protein in tissue responses to injuries from tumor necrosis factor and epilepsy.

Record Type:	Electronic resources : Monograph/item
Title/Author:	The role of the small heat shock protein in tissue responses to injuries from tumor necrosis factor and epilepsy./
Author:	Wang, Gang.
Description:	178 p.
Notes:	Source: Dissertation Abstracts International, Volume: 57-05, Section: B, page: 2995.
Contained By:	Dissertation Abstracts International57-05B.
Subject:	Biology, Cell. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9630033

The role of the small heat shock protein in tissue responses to injuries from tumor necrosis factor and epilepsy.
Wang, Gang.

The role of the small heat shock protein in tissue responses to injuries from tumor necrosis factor and epilepsy. - 178 p.

Source: Dissertation Abstracts International, Volume: 57-05, Section: B, page: 2995.

Thesis (Ph.D.)--University of Houston, 1996.

Tolerance is an interesting phenomenon observed in tissues responding to injurious stress. For example, an initial sublethal heat shock treatment may induce cells to become thermotolerant; sensitive tumor cells may become resistant to tumor necrosis factor (TNF) after exposure to a sublethal dose; and animal studies revealed that prior neural seizures conferred a time dependent protective effect against subsequent seizures. However, synthesis of heat shock proteins (hsp), a ubiquitous response to various injurious stresses, may play a common protective role in response to these stressors. Previous studies in our laboratory showed pretreatment of tumor cells with heat (which induces hsp) can reduce their sensitivity to TNF cytotoxicity. Of the major hsp families, the small heat shock protein (hsp27) is the most elusive in function and is reported to be upregulated by TNF and oxidative stress. We hypothesize that hsp27 may play a role in the tolerance response to TNF cytotoxicity and may be also expressed to respond to seizure attacks.Subjects--Topical Terms:

1017686
Biology, Cell.

The role of the small heat shock protein in tissue responses to injuries from tumor necrosis factor and epilepsy.
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100 1 $a Wang, Gang. $3 1258410
245 1 4 $a The role of the small heat shock protein in tissue responses to injuries from tumor necrosis factor and epilepsy.
300 $a 178 p.
500 $a Source: Dissertation Abstracts International, Volume: 57-05, Section: B, page: 2995.
500 $a Adviser: Dan E. Wells.
502 $a Thesis (Ph.D.)--University of Houston, 1996.
520 $a Tolerance is an interesting phenomenon observed in tissues responding to injurious stress. For example, an initial sublethal heat shock treatment may induce cells to become thermotolerant; sensitive tumor cells may become resistant to tumor necrosis factor (TNF) after exposure to a sublethal dose; and animal studies revealed that prior neural seizures conferred a time dependent protective effect against subsequent seizures. However, synthesis of heat shock proteins (hsp), a ubiquitous response to various injurious stresses, may play a common protective role in response to these stressors. Previous studies in our laboratory showed pretreatment of tumor cells with heat (which induces hsp) can reduce their sensitivity to TNF cytotoxicity. Of the major hsp families, the small heat shock protein (hsp27) is the most elusive in function and is reported to be upregulated by TNF and oxidative stress. We hypothesize that hsp27 may play a role in the tolerance response to TNF cytotoxicity and may be also expressed to respond to seizure attacks.
520 $a We successfully expressed human hsp27 in TNF sensitive murine cell lines, L929 and WEHI-164 and studied TNF cytotoxicity using neutral red, clonogenic, and chromium-release cytotoxicity assays. The results revealed that expression of hsp27 in TNF sensitive cells conferred significant resistance to TNF cytotoxicity and this protection is accompanied by the continued presence of hsp27 in the cells. Some sensitization is seen in ActD-treated hsp27-expressing cells compared with the non-ActD treated cells, suggesting other short-lived protective proteins may also exist to achieve the maximum protective function.
520 $a Phospholipase A2 (PLA2) activation induced by TNF causes increased arachidonic acid release and then consequently leads to increase intracellular oxyradical levels in sensitive cells. Our ( $\ sp3
520 $a Seizures also may be related to inappropriate reactive oxyradical releases. Epilepsy is a very common chronic disease with the feature of recurrent seizures. In the central nervous system, astrocytes are uniquely able to secrete TNF and have TNF receptors implying active hsp27 induction pathways exist. Yet, in the normal mammalian brain, hsp27 is not detectable by immunoblots. We also hypothesized that hsp27 is to protect cells ubiquitously from reactive oxyradicals, and should play a role in response to seizure attacks. Immunohistochemical studies revealed hsp27 was present in all the 15 surgical specimens tested from epilepsy patients and absent in all normal autopsy brain tissues. Double immunofluorescent staining showed hsp27 is expressed in some astrocyte specific protein (glial fibrillary acidic protein, GFAP) positive cells. Electron microscopic studies revealed hsp27 is localized in the cytoplasm of these cells. In situ hybridization of fresh surgically removed brain tissue from epilepsy patients also showed increased hsp27 mRNA in the astrocytes. (Abstract shortened by UMI.)
590 $a School code: 0087.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Health Sciences, Oncology. $3 1018566
690 $a 0379
690 $a 0307
690 $a 0317
690 $a 0992
710 2 0 $a University of Houston. $3 1019266
773 0 $t Dissertation Abstracts International $g 57-05B.
790 1 0 $a Wells, Dan E., $e advisor
790 $a 0087
791 $a Ph.D.
792 $a 1996
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9630033