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A genetic approach to study the regu...

Solle, Michael Edward.

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A genetic approach to study the regulation of inflammation by prostaglandin and extracellular nucleotide mediators.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	A genetic approach to study the regulation of inflammation by prostaglandin and extracellular nucleotide mediators./
作者:	Solle, Michael Edward.
面頁冊數:	218 p.
附註:	Director: Beverly H. Koller.
Contained By:	Dissertation Abstracts International63-08B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3061723
ISBN:	0493775994

A genetic approach to study the regulation of inflammation by prostaglandin and extracellular nucleotide mediators.
Solle, Michael Edward.

A genetic approach to study the regulation of inflammation by prostaglandin and extracellular nucleotide mediators. - 218 p.

Director: Beverly H. Koller.

Thesis (Ph.D.)--The University of North Carolina at Chapel Hill, 2002.

Inflammation occurs in response to many types of biological and physical stimuli. Small molecular mediators produced and released during inflammation constitute part of the first line of defense of the innate immune response. Two classes of these molecular mediators of inflammation are prostaglandins, which are derived from plasma membrane lipids, and nucleotides, which constitute part of the normal intracellular milieu. Both prostaglandin and nucleotide mediators bind to specific cell surface receptors that transduce a biochemical signal which in turn alters cellular function. This dissertation describes a genetic approach to study the role of these signaling molecules and their receptors.

ISBN: 0493775994Subjects--Topical Terms:

1017730
Biology, Genetics.

A genetic approach to study the regulation of inflammation by prostaglandin and extracellular nucleotide mediators.
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100 1 $a Solle, Michael Edward. $3 1250785
245 1 0 $a A genetic approach to study the regulation of inflammation by prostaglandin and extracellular nucleotide mediators.
300 $a 218 p.
500 $a Director: Beverly H. Koller.
500 $a Source: Dissertation Abstracts International, Volume: 63-08, Section: B, page: 3566.
502 $a Thesis (Ph.D.)--The University of North Carolina at Chapel Hill, 2002.
520 $a Inflammation occurs in response to many types of biological and physical stimuli. Small molecular mediators produced and released during inflammation constitute part of the first line of defense of the innate immune response. Two classes of these molecular mediators of inflammation are prostaglandins, which are derived from plasma membrane lipids, and nucleotides, which constitute part of the normal intracellular milieu. Both prostaglandin and nucleotide mediators bind to specific cell surface receptors that transduce a biochemical signal which in turn alters cellular function. This dissertation describes a genetic approach to study the role of these signaling molecules and their receptors.
520 $a Mast cells are versatile effector cells of the immune system whose activation has been implicated as contributing to inflammatory diseases. Mice deficient in E-series prostaglandin receptors EP1, EP2, EP 3, and EP4 were used to generate bone marrow derived mast cells and study the role of prostaglandins in regulating their function. We demonstrate that these mast cells are activated by PGE1 and PGE 2, inducing a potentiated degranulation response and increased cytokine IL-6 synthesis after IgE-antigen stimulation. In addition, we show that both of these effects are EP3-receptor dependent, and we demonstrate for the first time that the endogenous murine EP3 receptor couples to the mobilization of intracellular calcium.
520 $a Extracellular nucleotides bind with high affinity to specific cell surface P2 nucleotide receptors. The P2X7 receptor and the P2Y2 receptor have been specifically implicated as important receptors in mediating the inflammatory effects of extracellular nucleotides. Stimulation of the P2X7 receptor found on macrophages activates IL-1β posttranslational processing and release. Employing a genetic approach to inactivate the P2X 7 receptor we conclusively demonstrate that the P2X7 receptor is a necessary component for ATP stimulation of IL-1β processing and release. Stimulation of a P2Y2-like receptor on human neutrophils functionally activates them. Using mice genetically deficient in P2Y 2 receptors, we demonstrate that stimulation of this receptor mobilizes intracellular Ca<super>2+</super> and significantly potentiates superoxide production. Further, the receptor plays a significant role in the in vivo accumulation of neutrophils in a model of peritoneal inflammation. These findings demonstrate the emerging importance of nucleotide receptors as regulators of inflammation.
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710 2 0 $a The University of North Carolina at Chapel Hill. $3 1017449
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790 $a 0153
790 1 0 $a Koller, Beverly H., $e advisor
791 $a Ph.D.
792 $a 2002
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