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Journal of Dental Research
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Biological

Mechanism of Cyclosporine-induced Overgrowth in Gingiva

H.-J. Chae2, M.-S. Ha1, D.-H. Yun1, H.-O. Pae3, H.-T. Chung3, S.-W. Chae2, Y.-K. Jung4 and H.-R. Kim1,*

1 Department of Dental Pharmacology and Wonkwang Biomaterial Implant Research Institute, School of Dentistry, Wonkwang University, Iksan, Chonbuk, South Korea;
2 Department of Pharmacology and Institute of Cardiovascular Research, Medical School, Chonbuk National University, Jeonju, Chonbuk, South Korea;
3 Department of Microbiology and Immunology, School of Medicine, Wonkwang University, Iksan, Chonbuk, South Korea; and
4 Department of Biological Science, Seoul National University, Seoul, South Korea

Correspondence: * corresponding author, hrkimdp{at}wonkwang.ac.kr

Cyclosporine A (CsA) is a widely used immunosuppressant but with significant side-effects, such as gingival overgrowth. This study investigates how CsA induces gingival proliferation and shows the effects of the CsA-associated signaling messengers, IL-6 and TGF-β1, on gingival proliferation. CsA increased both IL-6 and TGF-β1 levels. In addition to CsA, an IL-6 or TGF-β1 treatment also induced gingival fibroblast proliferation. Inhibiting the cytokine resulted in the suppression of CsA-induced proliferation. MAPKs and PI3K are known to be involved in cell proliferation. Therefore, the effect of CsA on the kinase activities was examined. The results showed that both p38 MAPK and PI3K are essential for gingival fibroblast proliferation. TGF-β1 and IL-6 and their associated signaling transduction may be novel bona fide molecular targets for the prevention of gingival overgrowth in CsA-treated patients. (Abbreviations: MAPK, mitogen-activated protein kinase; PI3K, phosphatidylinositol 3-kinase.)

Key Words: Cyclosporine A • human gingival fibroblast

Journal of Dental Research, Vol. 85, No. 6, 515-519 (2006)
DOI: 10.1177/154405910608500607
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