The cDNA microarray study for the effect of FGF-5 administration on fibroblast

ABSTRACT

gingival hyperplasia was a common complication in organ transplantation patients. However, its exact mechanism had been remained unknown. In previous study, FGF-5 and FGF-7 were overexpressed in gingival hyperplasia. Here we analyzed the effect of FGF-5 on primary cultures of human fibroblast, grown in chemically defined medium, and we compared the proliferative and differentiative cell responses to FGF-5 with FGF-7. Cell counting and RT-PCR showed that FGF-5 was a potent mitogen for human fibroblasts. FGF-5 could up-regulated FGF-7 expression. However, FGF-7 down-regulated the expression of FGF-5 in human fibroblasts. In the cDNA microarray study, Nedd4 binding protein 3, epidermal growth factor receptor pathway substrate 15, transcription factor CP2, CDC20 cell division cycle 20 homolog, BRCA1 associated protein, and glutaminase were increased their expression after the administration of FGF-5. The pinin, ribosomal protein S29, proliferation-associated 2G4, protein phosphatase 1G, PICTAIRE protein kinase 1, cell division cycle 25A, keratin 7, 15, and 17, bone morphogenetic protein 1 and 7, and placental growth factor were In conclusion, FGF-5 was a potent mitogen for human fibroblasts, but FGF-7 was not. FGF-5 could induce FGF-7 expression, but FGF-7 inhibited FGF-5 expression. Thus, the gingival hyperplasia in the immunosuppressed patients seemed to be occurred via the action of FGF-5. The role of FGF-7 that was expressed in these patients might be late events after the expression of FGF-5.