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Novel mechanisms regulating cytokine-induced gene expression in astrocytes and glioblastoma cells.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
書名/作者:	Novel mechanisms regulating cytokine-induced gene expression in astrocytes and glioblastoma cells.
作者:	Bryan, Lauren Elizabeth.
面頁冊數:	199 p.
附註:	Source: Dissertation Abstracts International, Volume: 70-04, Section: B, page: 2064.
Contained By:	Dissertation Abstracts International70-04B.
標題:	Biology, Molecular.
標題:	Chemistry, Biochemistry.
ISBN:	9781109128505
摘要、提要註:	Chronic inflammation in the brain results in the development of several CNS diseases, including Alzheimer's and Parkinson's diseases, multiple sclerosis, and tumors. IL-1, a pro-inflammatory cytokine released by activated microglia and astrocytes, instigates the expression of factors promoting the progression of these CNS disorders, including cytokines, chemokines, and components of matrix remodeling systems, such as the plasminogen activator system. IL-1 also increases the mRNA expression and activity of SphK, the enzyme that phosphorylates Sph to form S1P, a bio-active sphingolipid. This thesis demonstrates that IL-1 and S1P enhance the mRNA and protein expression of PAI-1 and uPAR, two key components of the plasminogen activator system, in glioblastoma cells. The S1P-induced mRNA expression of PAI-1 and uPAR is mediated by the S1P2 receptor, and requires Rho-kinase and MEK1. However, IL-1 regulation of PAI-1 and uPAR mRNA expression is independent of SphK, and thus S1P. IL-1- and S1P-induced mRNA expression of PAI-1 and uPAR results in the increased in vitro invasion of glioblastoma cells. Since significant amounts of IL-1 are secreted from gliomas, and it increases the production of S1P via inciting the activity and mRNA expression of SphK, we propose a mechanism by which S1P and IL-1 influence the invasion of glioblastoma cells by increasing the mRNA and protein expression of uPAR and PAI-1.
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3356824

Novel mechanisms regulating cytokine-induced gene expression in astrocytes and glioblastoma cells.
Bryan, Lauren Elizabeth.

Novel mechanisms regulating cytokine-induced gene expression in astrocytes and glioblastoma cells. - 199 p.

Source: Dissertation Abstracts International, Volume: 70-04, Section: B, page: 2064.

Thesis (Ph.D.)--Virginia Commonwealth University, 2009.

Chronic inflammation in the brain results in the development of several CNS diseases, including Alzheimer's and Parkinson's diseases, multiple sclerosis, and tumors. IL-1, a pro-inflammatory cytokine released by activated microglia and astrocytes, instigates the expression of factors promoting the progression of these CNS disorders, including cytokines, chemokines, and components of matrix remodeling systems, such as the plasminogen activator system. IL-1 also increases the mRNA expression and activity of SphK, the enzyme that phosphorylates Sph to form S1P, a bio-active sphingolipid. This thesis demonstrates that IL-1 and S1P enhance the mRNA and protein expression of PAI-1 and uPAR, two key components of the plasminogen activator system, in glioblastoma cells. The S1P-induced mRNA expression of PAI-1 and uPAR is mediated by the S1P2 receptor, and requires Rho-kinase and MEK1. However, IL-1 regulation of PAI-1 and uPAR mRNA expression is independent of SphK, and thus S1P. IL-1- and S1P-induced mRNA expression of PAI-1 and uPAR results in the increased in vitro invasion of glioblastoma cells. Since significant amounts of IL-1 are secreted from gliomas, and it increases the production of S1P via inciting the activity and mRNA expression of SphK, we propose a mechanism by which S1P and IL-1 influence the invasion of glioblastoma cells by increasing the mRNA and protein expression of uPAR and PAI-1.

ISBN: 9781109128505Subjects--Topical Terms:

422925
Biology, Molecular.

Novel mechanisms regulating cytokine-induced gene expression in astrocytes and glioblastoma cells.
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245 1 0 $a Novel mechanisms regulating cytokine-induced gene expression in astrocytes and glioblastoma cells.
300 $a 199 p.
500 $a Source: Dissertation Abstracts International, Volume: 70-04, Section: B, page: 2064.
500 $a Adviser: Tomasz Kordula.
502 $a Thesis (Ph.D.)--Virginia Commonwealth University, 2009.
520 $a Chronic inflammation in the brain results in the development of several CNS diseases, including Alzheimer's and Parkinson's diseases, multiple sclerosis, and tumors. IL-1, a pro-inflammatory cytokine released by activated microglia and astrocytes, instigates the expression of factors promoting the progression of these CNS disorders, including cytokines, chemokines, and components of matrix remodeling systems, such as the plasminogen activator system. IL-1 also increases the mRNA expression and activity of SphK, the enzyme that phosphorylates Sph to form S1P, a bio-active sphingolipid. This thesis demonstrates that IL-1 and S1P enhance the mRNA and protein expression of PAI-1 and uPAR, two key components of the plasminogen activator system, in glioblastoma cells. The S1P-induced mRNA expression of PAI-1 and uPAR is mediated by the S1P2 receptor, and requires Rho-kinase and MEK1. However, IL-1 regulation of PAI-1 and uPAR mRNA expression is independent of SphK, and thus S1P. IL-1- and S1P-induced mRNA expression of PAI-1 and uPAR results in the increased in vitro invasion of glioblastoma cells. Since significant amounts of IL-1 are secreted from gliomas, and it increases the production of S1P via inciting the activity and mRNA expression of SphK, we propose a mechanism by which S1P and IL-1 influence the invasion of glioblastoma cells by increasing the mRNA and protein expression of uPAR and PAI-1.
520 $a IL-1 and S1P also influence the mRNA expression of chemokines implicated in the development and progression of multiple sclerosis, namely IP-10 and RANTES, in primary human astrocytes. IP-10 and RANTES attract T cells, which are the major pathological cause of multiple sclerosis. This thesis demonstrates a novel mechanism by which S1P significantly inhibits the IL-1-induced mRNA expression of these chemokines. The mechanism by which S1P reduces IL-1-induced IP-10 and RANTES mRNA expression involves the prolonged hyperphosphorylation of TAK1, as well as the inhibition of IL-1-stimulated IFNbeta production and the phosphorylation of STAT1 and STAT2.
520 $a In summary, this dissertation describes the mechanisms by which S1P and IL-1 control the mRNA expression of two chemokines associated with multiple sclerosis, and the components of the plasminogen activator system, which are critical for the invasion of glioblastoma cells; thus, indicating future therapeutic targets for destructive CNS disorders.
590 $a School code: 2383.
650 4 $a Biology, Molecular. $3 422925
650 4 $a Chemistry, Biochemistry. $3 422931
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690 $a 0487
710 2 $a Virginia Commonwealth University. $3 422997
773 0 $t Dissertation Abstracts International $g 70-04B.
790 1 0 $a Kordula, Tomasz, $e advisor
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791 $a Ph.D.
792 $a 2009
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