The mRNA expression of MMP-1, TIMP-1, TGF-beta1 in gingival keratocytes from gingival hyperplasia induced by cyclosporine A.
- Author:
Hag Soo KANG
1
;
Jae Sun LEE
;
Jung Ho BING
;
Chang Joo PARK
;
Jae Jung IM
;
Kyung Gyun HWANG
;
Kwang Sup SHIM
Author Information
1. Division of Oral and Maxillofacial Surgery/Department of Dentistry, College of Medicine, Hanyang University, Korea. hkg@hanyang.ac.kr
- Publication Type:Original Article
- Keywords:
MMP-1;
TIMP-1;
TGF-beta1;
cyclosporine A;
gingival keratinocyte
- MeSH:
Autoimmune Diseases;
Collagen;
Cyclosporine;
Gingival Hyperplasia;
Graft Rejection;
Humans;
Keratinocytes;
RNA, Messenger;
Tissue Donors;
Tissue Inhibitor of Metalloproteinase-1;
Transforming Growth Factor beta1
- From:Journal of the Korean Association of Oral and Maxillofacial Surgeons
2008;34(4):405-411
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Cyclosporine A (CsA) is a versatile immunosuppresive agent used to prevent graft rejection syndrome and treat autoimmune disease. One of the major side effects associated with CsA is the abnormal gingival hyperplasia. The purpose of this study was to investigate the relationship between the mRNA expression of the MMP-1, TIMP-1, and TGF-beta1 and the concentration of CsA in cultured human gingival keratinocytes. MATERIALS AND METHODS: Gingival keratocytes were obtained from gingival tissues of 4 healthy donors. The cultured gingival keratocytes were incubated with increasing concentrations of CsA (0-2000 ng/ml) for 24 hours and the expression of MMP-1, TIMP-1, and TGF-beta1 were determined by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The expressions of MMP-1 and TGF-beta1 were not significantly different according to the concentrations of CsA. The expression of TIMP-1 was significantly increased at the CsA concentration of 500 ng/ml. CONCLUSION: We concluded that the gingival hyperplasia induced by CsA was more related with TIMP-1 than MMP-1 or TGF-beta1 on gingival collagen metabolism in patients treated with CsA.
