P. gingivalis Regulates the Expression of Cathepsin B and Cystatin C

Porphyromonas gingivalis is a major etiological agent of periodontitis that could affect the expression of Cathepsins B and C by disrupting the balance between these enzymes and their inhibitor, Cystatin C. We tested this hypothesis by infecting human oral epithelial cells with P. gingivalis or acti...

Full description

Saved in:
Bibliographic Details
Published in:Journal of dental research 2008-10, Vol.87 (10), p.932-936
Main Authors: Elkaim, R., Werner, S., Kocgozlu, L., Tenenbaum, H.
Format: Article
Language:English
Subjects:
Blotting, Western
Cathepsin B - biosynthesis
Cathepsin C - biosynthesis
Cell Line, Transformed
Cystatin C - antagonists & inhibitors
Dentistry
Down-Regulation
Humans
Keratinocytes - microbiology
Lipopolysaccharides
Porphyromonas gingivalis - physiology
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - biosynthesis
Up-Regulation
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Porphyromonas gingivalis is a major etiological agent of periodontitis that could affect the expression of Cathepsins B and C by disrupting the balance between these enzymes and their inhibitor, Cystatin C. We tested this hypothesis by infecting human oral epithelial cells with P. gingivalis or activating solely by its lipopolysaccharide. The mRNA level, the enzymatic activity, and the protein expression of Cathepsin B were increased (three-fold) in a dose-dependent manner, while those of Cystatin C decreased (five-fold). No changes were observed for Cathepsin C. Although activation by lipopolysaccharides led to a delayed imbalance (2 days) between Cathepsin B and Cystatin C, this imbalance took place very rapidly during the infection (< 6 hrs), indicating that the whole bacterium contains components that initiate rapid changes in the transcription rates of Cathepsin B and Cystatin C and selectively modify the molecular pathways that lead to this imbalance.
ISSN:0022-0345
1544-0591
DOI:10.1177/154405910808701010