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Journal of Dental Research
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Biological

Re-oxygenation Improves Hypoxia-induced Pulp Cell Arrest

Y. Ueno1, C. Kitamura1, M. Terashita1 and T. Nishihara2,*

1 Division of Pulp Biology, Operative Dentistry, and Endodontics, Department of Cariology and Periodontology, Science of Oral Functions, and
2 Division of Infections and Molecular Biology, Department of Health Promotion, Science of Health Improvement, Kyushu Dental College, 2-6-1 Manazuru, Kokurakita, Kitakyushu 803-8580, Japan

Correspondence: * corresponding author, tatsujin{at}kyu-dent.ac.jp

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 p21CIP1/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.

Key Words: hypoxia • cell-cycle arrest • re-oxygenation • dental pulp cells

Journal of Dental Research, Vol. 85, No. 9, 824-828 (2006)
DOI: 10.1177/154405910608500909
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