Inhibition of phosphatidylinositol 3-kinase amplifies TEGDMA-induced apoptosis in primary human pulp cells

Spagnuolo, G. and Galler, K. and Schmalz, G. and Cosentino, C. and Rengo, S. and Schweikl, Helmut (2004) Inhibition of phosphatidylinositol 3-kinase amplifies TEGDMA-induced apoptosis in primary human pulp cells. JOURNAL OF DENTAL RESEARCH, 83 (9). pp. 703-707. ISSN 0022-0345, 1544-0591

Full text not available from this repository. (Request a copy)

Abstract

Cytotoxicity of triethylene glycol dimethacrylate ( TEGDMA), a co- monomer of dental resinous restorative materials, is firmly established in vitro, but the molecular mechanisms are unknown. Here we examined apoptosis and necrosis induced by TEGDMA in human primary pulp cells. The levels of apoptotic and necrotic cell populations differentially increased after exposure to increasing concentrations of TEGDMA. A twofold increase in the percentage of apoptotic cells was induced by 1 mmol/ L TEGDMA. However, a population shift among cells in apoptosis and necrosis was detected when cell cultures were exposed to 2 mmol/ L TEGDMA. Inhibition of the MAP Kinase/ ERK pathway had no influence on cell survival, but inhibition of phosphatidylinositol 3 kinase ( PI3- Kinase; Akt/ protein kinase B) by LY294002 amplified TEGDMA- induced apoptosis. Moreover, Akt phosphorylation was inhibited in the presence of TEGDMA. These results suggest that depression of PI3K signaling may be a primary target in TEGDMA- induced apoptosis.

Item Type: Article
Uncontrolled Keywords: HUMAN GINGIVAL FIBROBLASTS; SIGNALING PATHWAYS; PROTEIN-KINASES; C-JUN; COMPONENTS; DEATH; DENTINOGENESIS; EXPRESSION; INDUCTION; SURVIVAL; pulp cells; apoptosis; necrosis; TEGDMA; PI3K
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Zahnerhaltung und Parodontologie > Prof. Dr. rer. nat. Helmut Schweikl
Depositing User: Dr. Gernot Deinzer
Date Deposited: 30 Jun 2021 08:48
Last Modified: 30 Jun 2021 08:48
URI: https://pred.uni-regensburg.de/id/eprint/37268

Actions (login required)

View Item View Item