Re-oxygenation improves hypoxia-induced pulp cell arrest.

Abstract

Dental pulp cells can be exposed to hypoxia during severe inflammation or restorative procedures, though their response to hypoxia is not well-understood. We hypothesized that hypoxia has effects on the growth of pulp cells in vitro. When the cells were exposed to hypoxia for 48 hr, cell growth was suppressed, and cell death was detected by Hoechst staining. Western blot analysis revealed that phosphorylation of retinoblastoma protein was inhibited in cells exposed to hypoxia. Analyses of the molecules involved in retinoblastoma protein phosphorylation revealed that hypoxia suppressed cyclin D2 and activated p21(CIP1/WAF1). Further, hypoxia-exposed pulp cells showed improvement of cell viability, cell-cycle progression, and expression of cyclin D2 with re-oxygenation. These findings indicate that hypoxia-induced cell cycle arrest in pulp cells is reversible, while cyclin D2 may play an essential role in the improvement of cell proliferation with re-oxygenation.

• Authors: Y Ueno, C Kitamura, M Terashita, T Nishihara
• Journal: Journal of dental research (J Dent Res) Vol. 85 Issue 9 Pg. 824-8 (Sep 2006) ISSN: 0022-0345 [Print] United States
• PMID: 16931865 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Ccnd2 protein, rat
• Cdkn1a protein, rat
• Cyclin D2
• Cyclin-Dependent Kinase Inhibitor p21
• Cyclins
• Retinoblastoma Protein
• Oxygen

Topics

• Analysis of Variance
• Animals
• Apoptosis (drug effects, physiology)
• Blotting, Western
• Cell Cycle (drug effects)
• Cell Hypoxia (physiology)
• Cell Survival (drug effects)
• Cells, Cultured
• Cyclin D2
• Cyclin-Dependent Kinase Inhibitor p21 (metabolism)
• Cyclins (metabolism)
• Dental Pulp (cytology, metabolism)
• Oxygen (pharmacology)
• Phosphorylation
• Rats
• Retinoblastoma Protein (metabolism)