Objective：To investigate the effect of nifedipine（calciumchannel blocker） on the expression of collagen in gingival fibroblasts invitro. Methods：Primarily gingival fibroblasts were cultured and incubated with vari...Objective：To investigate the effect of nifedipine（calciumchannel blocker） on the expression of collagen in gingival fibroblasts invitro. Methods：Primarily gingival fibroblasts were cultured and incubated with various concentrations of nifedipine（108 μg/L, 360 μg/L and 1200 μg/L）for 5 days. Gingival fibroblasts were primarily cultured derived from nifedipine responders and nonresponders in the presence of 360 μg/L nifedipine. Enzyme-linked immunosorbent assay was used to evaluate the amount of type I collagen. Cell proliferation was measured by cell counting with evaluating MTT value. Results：The expressions of collagen and cell proliferation were significantly different among the high concentration groups and the others on the fifth day, especially higher in 360 μg/L and 1200 μg/L groups and also different among nifedipine responders and non-responders. Conclusion：The expression of collagen and cell proliferation may be concerned with the biological mechanism for gingival overgrowth.展开更多
Background: Among anti-hypertension drugs, calcium (Ca2+) antagonists cause gingival overgrowth as a side effect. We previously discovered that this side effect was due to elevation of the calcium concentration in the...Background: Among anti-hypertension drugs, calcium (Ca2+) antagonists cause gingival overgrowth as a side effect. We previously discovered that this side effect was due to elevation of the calcium concentration in the cytosol ([Ca2+]i). Ca2+ entry through non-selective cation channels (NSCCs) and Ca2+ release from intracellular Ca2+ stores are involved in this [Ca2+]i elevation. Furthermore, we discovered that calcium-sensing receptors (CaSRs) participate in nifedipine-induced [Ca2+]i elevation. Transient receptor potential (TRP) channels have been identified as NSCCs. In the present study, we undertook experiments to determine if TRPV1 channels are present in gingival fibroblasts and to ascertain if nifedipine-activated NSCCs are TRPV1 channels. Methods Normal human gingival fibroblast Gin-1 cells were used. The [Ca2+]i was measured using a video-imaging analysis system with the Ca2+-sensitive fluorescent dye fura-2/AM. Results: The NSCC inhibitor SKF96365 significantly inhibited nifedipine-induced [Ca2+]i elevation. TRPV1 channel agonists such as capsaicin, olvanil and resiniferatoxin concentration-dependently elevated the [Ca2+]i. The TRPV1 channel activator anandamide concentration-dependently increased the [Ca2+]i. The TRPV1 channel antagonists capsazepine, AMG9810, iodoresiniferatoxin, ruthenium red, and SB366791 significantly inhibited nifedipine-induced [Ca2+]i elevation. Conclusion: These results suggest that Ca2+ entry through TRPV1 channels is involved in the nifedipine-induced [Ca2+]i elevation seen in gingival fibroblasts. We describe here a modified version of our ‘calcium trigger theory’.展开更多
基金suppored by the Natural Science Foundation of the Department of Education of Jiangsu(BK2006172)
文摘Objective：To investigate the effect of nifedipine（calciumchannel blocker） on the expression of collagen in gingival fibroblasts invitro. Methods：Primarily gingival fibroblasts were cultured and incubated with various concentrations of nifedipine（108 μg/L, 360 μg/L and 1200 μg/L）for 5 days. Gingival fibroblasts were primarily cultured derived from nifedipine responders and nonresponders in the presence of 360 μg/L nifedipine. Enzyme-linked immunosorbent assay was used to evaluate the amount of type I collagen. Cell proliferation was measured by cell counting with evaluating MTT value. Results：The expressions of collagen and cell proliferation were significantly different among the high concentration groups and the others on the fifth day, especially higher in 360 μg/L and 1200 μg/L groups and also different among nifedipine responders and non-responders. Conclusion：The expression of collagen and cell proliferation may be concerned with the biological mechanism for gingival overgrowth.
文摘Background: Among anti-hypertension drugs, calcium (Ca2+) antagonists cause gingival overgrowth as a side effect. We previously discovered that this side effect was due to elevation of the calcium concentration in the cytosol ([Ca2+]i). Ca2+ entry through non-selective cation channels (NSCCs) and Ca2+ release from intracellular Ca2+ stores are involved in this [Ca2+]i elevation. Furthermore, we discovered that calcium-sensing receptors (CaSRs) participate in nifedipine-induced [Ca2+]i elevation. Transient receptor potential (TRP) channels have been identified as NSCCs. In the present study, we undertook experiments to determine if TRPV1 channels are present in gingival fibroblasts and to ascertain if nifedipine-activated NSCCs are TRPV1 channels. Methods Normal human gingival fibroblast Gin-1 cells were used. The [Ca2+]i was measured using a video-imaging analysis system with the Ca2+-sensitive fluorescent dye fura-2/AM. Results: The NSCC inhibitor SKF96365 significantly inhibited nifedipine-induced [Ca2+]i elevation. TRPV1 channel agonists such as capsaicin, olvanil and resiniferatoxin concentration-dependently elevated the [Ca2+]i. The TRPV1 channel activator anandamide concentration-dependently increased the [Ca2+]i. The TRPV1 channel antagonists capsazepine, AMG9810, iodoresiniferatoxin, ruthenium red, and SB366791 significantly inhibited nifedipine-induced [Ca2+]i elevation. Conclusion: These results suggest that Ca2+ entry through TRPV1 channels is involved in the nifedipine-induced [Ca2+]i elevation seen in gingival fibroblasts. We describe here a modified version of our ‘calcium trigger theory’.
