THE ROLE OF MITOCHONDRIAL CALCIUM OVERLOAD IN CYCLOSPORINE A-INDUCED GINGIVAL HYPERPLASIA
Ancuţa Goriuc, Bogdan Minea, Foia Liliana, Marcel Costuleanu, Raluca Jipu, Vasilica Toma, Vlad Cristiana, Ionuţ Luchian, Ioana Mârţu
Aim of the study Apoptosis (programmed cell death) is a possible mechanism of cyclosporine A (CsA)-induced gingival hyperplasia. The purpose of this paper is to study the effect of ionomycin and ionophore A23187 on normal gingival fibroblasts and also on fibroblasts treated with CsA using flow cytometry methods. Material and methods All of our experiments were performed on fibroblasts obtained from gingival male rats through explant technique and the opening of the mitochondrial transient permeability pore as a result of calcium cytosol overload was followed using calcein AM and CoCl2. Results Our results show a significant difference between normal gingival fibroblasts and those treated with CsA when using ionophore A23187. On the other hand, ionomycin hasn’t significant effects on mitochondrial calcein load in normal or treated fibroblasts. Conclusions: Cytosolic calcium overload is one of the mechanisms involved in drug-induced gingival hyperplasia.
Key words: apoptosis, gingival overgrowth, calcein, flow cytometry, cyclosporine Aapoptosis, calcein, cyclosporine A, flow cytometry, gingival overgrowth