Induction of tissue plasminogen activator gene expression by proinflammatory cytokines in human pulp and gingival fibroblasts

doi:10.1097/00004770-200302000-00007

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 310902500/18379

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/18379

Title:	Induction of tissue plasminogen activator gene expression by proinflammatory cytokines in human pulp and gingival fibroblasts
Authors:	Chang, Y.-C.;Yang, S.-F.;Huang, F.-M.;Tai, K.-W.;Hsieh, Y.-S.
Date:	2003
Issue Date:	2017-08-14T08:49:41Z (UTC)
ISSN:	0099-2399
Abstract:	Plasminogen activator converts plasminogen to plasmin, and plasmin activates the latent matrix metalloproteinases. Tissue plasminogen activator (t-PA) is one of the important proteolysis factors present in human inflamed tissues. However, few studies reported on the mechanisms of tissue destruction via a t-PA proteolysis pathway in pulpal and periapical diseases. The subsequent reactions leading to pulpal and periapical injury after the induction of proinflammatory cytokines remains to be elucidated. The aim of this study was to investigate the effects of interleukin-1α and tumor necrosis factor-α on the expression of t-PA mRNA gene in cultured human pulp and gingival fibroblasts. The mRNAs for t-PA were measured by reverse transcription-polymerase chain reaction at 2, 6, and 24 h. The results show that both cytokines induced significantly high levels of t-PA mRNA gene expression in human pulp fibroblasts. The peak of t-PA mRNA levels induced by both proinflammatory cytokines was at the 6-h incubation period. Interleukin-1α was found to be more effective in induction of t-PA gene expression than tumor necrosis factor-α. In addition, a similar induction pattern was also found in human gingival fibroblasts. These results indicate that proinflammatory cytokines can induce t-PA gene expression and such an effect may partially contribute to the destruction of pulpal and periapical tissues through dysregulated pericellular proteolysis. An understanding of the mechanism could not only further define the role of immune events in pulpal and periapical diseases but also have important implication for pharmacological intervention. Copyright © 2003 by The American Association of Endodontists.
URI:	http://dx.doi.org/10.1097/00004770-200302000-00007 https://www.scopus.com/inward/record.uri?eid=2-s2.0-0038823931&doi=10.1097%2f00004770-200302000-00007&partnerID=40&md5=d000ceb02c5e73e6c9d00df781136806 https://ir.csmu.edu.tw:8080/ir/handle/310902500/18379
Relation:	Journal of Endodontics 29 (2) ,114-117
Appears in Collections:	[牙醫學系暨碩士班] 期刊論文

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