Examination of the signal transduction pathways leading to upregulation of tissue type plasminogen activator by interleukin-1alpha in human pulp cells.

doi:10.1016/j.joen.2005.10.004

中山醫學大學機構典藏 CSMUIR > 口腔醫學院 > 牙醫學系暨碩士班 > 期刊論文 > Item 310902500/10587

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/10587

Title:	Examination of the signal transduction pathways leading to upregulation of tissue type plasminogen activator by interleukin-1alpha in human pulp cells.
Authors:	Huang, FM Tsai, CH Chen, YJ Chou, MY Chang, YC
Contributors:	中山醫學大學
Date:	2006
Issue Date:	2015-04-10T04:53:08Z (UTC)
ISSN:	0099-2399
Abstract:	Tissue type plasminigen activator (t-PA) is one of the important proteolysis factors in the pathogenesis of pulpal inflammation. However, the mechanisms and signal transduction pathways involved in the production of t-PA in human pulp cells are not fully understood. The purpose of this study was to investigate the t-PA activity in human pulp cells stimulated with various pharmacological agents. IL-1alpha was used to evaluate t-PA activity in human pulp cells using casein zymography and enzyme-linked immunosorbent assay (ELISA). Furthermore, to search possible signal transduction pathways, p38 inhibitor SB203580, MEK inhibitor U0126, and phosphatidylinositaol 3-kinase (PI3K) inhibitor LY294002 were added to test how they modulated the t-PA activity. The main casein secreted by human pulp cells migrated at 70 kDa and represented t-PA. Secretion of t-PA was found to be stimulated with IL-1alpha during 2 day cultured period (p < 0.05). From the results of casein zymography and ELISA, SB203580, U0126, and LY294002 significantly reduced the IL-1alpha-stimulated t-PA production, respectively (p < 0.05). Our findings demonstrated that IL-1alpha enhance t-PA production in human pulp cells, and the signal transduction pathways p38, MEK, and PI3K are involved in the inhibition of t-PA. SB203580, U0126, and LY294002 suppress t-PA activity and may also have important implication for pharmacological intervention.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/10587 http://dx.doi.org/10.1016/j.joen.2005.10.004
Relation:	J Endod. 2006 Jan;32(1):30-3.
Appears in Collections:	[牙醫學系暨碩士班] 期刊論文

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