J Korean Assoc Maxillofac Plast Reconstr Surg.  2006 Sep;28(5):445-453.

The mRNA expression of growth factors in fibroblast from gingival hyperplasia induced by cyclosporine A

• Kim YM
• Hwang KG
• Lee JS

Abstract

Cyclosporine A (CsA) is a powerful immunosuppresive agent used to prevent graft rejection of organ and treat autoimmune disease. One of the major side effects associated with CsA treatment is the development of gingival overgrowth. The purpose of this study was to investigate the mRNA expression and association of the several growth factors in gingival overgrowth induced by CsA, respectively. Gingival fibroblasts were obtained from gingival tissues of healthy donor and the patients treated with CsA. The cultured gingival fibroblasts were incubated with increasing concentrations of CsA for 24 hours, and the expression of MMP-1, TIMP-1, TGF-beta1, p21 were determined by reverse transcription-polymerase chain reaction (RT-PCR). The expressions of MMP-1 was slightly increased according to the concentration of treated CsA, but there was no statistical significance. TIMP-1 showed the increased expression at the CsA concentration of 250 and 500 ng/ml and significantly decreased at the CsA concentration of 750ng/ml. TGF-beta1 showed the increased expression at the CsA concentration of 500 and 750 ng/ml. The expression of p21 was not changed significantly. We concluded that the gingival hyperplasia induced by CsA was more related with TGF-beta1 than MMP-1 or TIMP-1 on gingival collagen metabolism in patients treated with CsA.

Keyword

MMP-1; TIMP-1; TGF-beta1; p21; Cyclosporine A

MeSH Terms

Autoimmune Diseases
Collagen
Cyclosporine*
Fibroblasts*
Gingival Hyperplasia*
Gingival Overgrowth
Graft Rejection
Humans
Intercellular Signaling Peptides and Proteins*
Metabolism
RNA, Messenger*
Tissue Donors
Tissue Inhibitor of Metalloproteinase-1
Transforming Growth Factor beta1
Collagen
Cyclosporine
Intercellular Signaling Peptides and Proteins
RNA, Messenger
Tissue Inhibitor of Metalloproteinase-1
Transforming Growth Factor beta1