Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/60626
Citations | ||
Scopus | Web of Science® | Altmetric |
---|---|---|
?
|
?
|
Type: | Journal article |
Title: | Inhibition of apoptosis in periodontitis |
Author: | Lucas, H. Bartold, P. Dharmapatni, A. Holding, C. Haynes, D. |
Citation: | Journal of Dental Research, 2010; 89(1):29-33 |
Publisher: | Inter Amer Assoc Dental Research |
Issue Date: | 2010 |
ISSN: | 0022-0345 1544-0591 |
Statement of Responsibility: | H. Lucas, P.M. Bartold, A.A.S.S.K. Dharmapatni, C.A. Holding and D.R. Haynes |
Abstract: | This study investigated whether the prolonged survival of inflammatory cells in periodontal disease could be due to the inhibition of apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) decoy receptors and inhibition of the terminal stages of apoptosis signaling by inhibitor of apoptosis (IAP) family members. Gingival tissue samples were taken from healthy individuals and those with chronic periodontitis. The expression of TRAIL, TRAIL receptors, TUNEL, cleaved caspase-3, xIAP, and survivin was determined immunohistologically and at the level of mRNA expression. Higher levels of TRAIL and the TRAIL decoy receptor, TRAIL R4, were expressed in the diseased periodontal tissues (p < 0.005). Statistically (p < 0.05) higher levels of cleaved caspase-3 and the cleaved caspase-3 inhibitors, xIAP and survivin, were seen. Similar changes were seen at the level of mRNA. The results indicate that apoptosis in periodontitis may be inhibited by elevated expression of TRAIL decoy receptors and cleaved caspase-3 inhibitors. |
Keywords: | apoptosis TRAIL caspase-3 xIAP survivin. |
Rights: | Copyright © 2010 by International & American Associations for Dental Research |
DOI: | 10.1177/0022034509350708 |
Grant ID: | NHMRC |
Published version: | http://dx.doi.org/10.1177/0022034509350708 |
Appears in Collections: | Aurora harvest 5 Pathology publications |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.