Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/38956
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Type: Journal article
Title: Effect of lipopolysaccharide from periodontal pathogens on the production of tissue plasminogen activator and plasminogen activator inhibitor 2 by human gingival fibroblasts
Author: Xiao, Y.
Bunn, C.
Bartold, P.
Citation: Journal of Periodontal Research, 2001; 36(1):25-31
Publisher: Blackwell Munksgaard
Issue Date: 2001
ISSN: 0022-3484
1600-0765
Statement of
Responsibility: 
Yin Xiao, Clive L. Bunn, P. Mark Bartold
Abstract: Both tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 2 (PAI-2) are important proteolysis factors present in inflamed human periodontal tissues. The aim of the present study was to investigate the effect of lipopolysaccharide (LPS) on the synthesis of t-PA and PAI-2 by human gingival fibroblasts (HGF). LPS from different periodontal pathogens including Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and Fusobacterium nucleatum were extracted by the hot phenol water method. The levels of t-PA and PAI-2 secreted into the cell culture media were measured by enzyme-linked immunosorbent assays (ELISA). The mRNA for t-PA and PAI-2 were measured by RT-PCR. The results showed t-PA synthesis was increased in response to all types of LPS studied and PAI-2 level was increased by LPS from A. actinomycetemcomitans and F. nucleatum, but not P. gingivalis. When comparing the effects of LPS from non-periodontal bacteria (Escherichia coli and Salmonella enteritidis) with the LPS from periodontal pathogens, we found that the ratio of t-PA to PAI-2 was greater following exposure of the cells to LPS from periodontal pathogens. The highest ratio of t-PA to PAI-2 was found in those cells exposed to LPS from P. gingivalis. These results indicate that LPS derived from periodontal pathogens may cause unbalanced regulation of plasminogen activator and plasminogen activator inhibitor by HGF and such an effect may, in part, contribute to the destruction of periodontal connective tissue through dysregulated pericellular proteolysis.
Keywords: plasminogen activator
plasminogen activator inhibitor
fibroblasts
lipopolysaccharide
periodontal
Description: The definitive version is available at www.blackwell-synergy.com
DOI: 10.1034/j.1600-0765.2001.00608.x
Appears in Collections:Aurora harvest 6
Dentistry publications

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