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

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-1alpha and tumor necrosis factor-alpha 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-1alpha was found to be more effective in induction of t-PA gene expression than tumor necrosis factor-alpha. 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.

journal_name

J Endod

journal_title

Journal of endodontics

authors

Chang YC,Yang SF,Huang FM,Tai KW,Hsieh YS

doi

10.1097/00004770-200302000-00007

keywords:

subject

Has Abstract

pub_date

2003-02-01 00:00:00

pages

114-7

issue

2

eissn

0099-2399

issn

1878-3554

pii

S0099-2399(05)60546-8

journal_volume

29

pub_type

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