摘要
Background Rosiglitazone is known as the most potent and specific peroxisome proliferators-activated receptor γ （PPAR-γ） ligand. It has potentially far-reaching effects on pathophysiological processes, from cancer to atherosclerosis and diabetes. However, it is not clear whether rosiglitazone affects the protein expression of transforming growth factor β3 （TGF-β3） and the cell proliferation in human uterine leiomyoma cells in vitro.Methods Human uterine leiomyoma tissues were dissected and cultured. Cells were divided into 5 groups： one control group and other four groups with different concentrations of rosiglitazone （10^-7, 10^-8, 10^-9 and 10^-10 mol/L）. Cells were cultured for 72 hours in serum-free Dulbecco＇s modified Eagle＇s medium. MTT reduction assay was used to detect the cell proliferation. Reverse transcription polymerase chain reaction （RT-PCR） was used to detect the mRNA expression of PPAR-γ and TGF-β3. Immunofluorescence staining was used to detect the expressions of PPAR-γ and TGF-β3 proteins. Results MTT reduction assay indicated that the treatment with rosiglitazone （from 10^-7 to 10^-9 mol/L） resulted in an inhibition of the cell growths after 72 hours （P〈0.01）. RT-PCR analysis revealed that 10^-7 mol/L rosiglitazone significantly affected the gene expression at 72-hour： PPAR-γ mRNA expression was up-regulated and TGF-β3 mRNA was down-regulated and rosiglitazone at the concentration of 10-7 mol/L affected these most effectively （P〈0.01）. Immunofluorescence staining demonstrated that treatment with 10^-7 mol/L rosiglitazone resulted in the significant changes of PPAR-γ and TGF-β3 protein expressions compared with the other treatment groups and the control group at 72-hour （P〈0.01）. All the effects of rosiglitazone on uterine leiomyoma cells were dose- and time-dependent in vitro. Conclusions The present study demonstrates that the PPAR-γ activator, rosiglitazone, inhibits the cell proliferation partly through the regulations of PPAR-γ and TGF-β3 expressions. The cross-talk between the signal pathways of PPAR-γ and TGF-β3 may be involved in the process.
Background Rosiglitazone is known as the most potent and specific peroxisome proliferators-activated receptor γ （PPAR-γ） ligand. It has potentially far-reaching effects on pathophysiological processes, from cancer to atherosclerosis and diabetes. However, it is not clear whether rosiglitazone affects the protein expression of transforming growth factor β3 （TGF-β3） and the cell proliferation in human uterine leiomyoma cells in vitro.Methods Human uterine leiomyoma tissues were dissected and cultured. Cells were divided into 5 groups： one control group and other four groups with different concentrations of rosiglitazone （10^-7, 10^-8, 10^-9 and 10^-10 mol/L）. Cells were cultured for 72 hours in serum-free Dulbecco＇s modified Eagle＇s medium. MTT reduction assay was used to detect the cell proliferation. Reverse transcription polymerase chain reaction （RT-PCR） was used to detect the mRNA expression of PPAR-γ and TGF-β3. Immunofluorescence staining was used to detect the expressions of PPAR-γ and TGF-β3 proteins. Results MTT reduction assay indicated that the treatment with rosiglitazone （from 10^-7 to 10^-9 mol/L） resulted in an inhibition of the cell growths after 72 hours （P〈0.01）. RT-PCR analysis revealed that 10^-7 mol/L rosiglitazone significantly affected the gene expression at 72-hour： PPAR-γ mRNA expression was up-regulated and TGF-β3 mRNA was down-regulated and rosiglitazone at the concentration of 10-7 mol/L affected these most effectively （P〈0.01）. Immunofluorescence staining demonstrated that treatment with 10^-7 mol/L rosiglitazone resulted in the significant changes of PPAR-γ and TGF-β3 protein expressions compared with the other treatment groups and the control group at 72-hour （P〈0.01）. All the effects of rosiglitazone on uterine leiomyoma cells were dose- and time-dependent in vitro. Conclusions The present study demonstrates that the PPAR-γ activator, rosiglitazone, inhibits the cell proliferation partly through the regulations of PPAR-γ and TGF-β3 expressions. The cross-talk between the signal pathways of PPAR-γ and TGF-β3 may be involved in the process.
基金
This work was supported by the Natural Science Foundation of Shandong Province （No.Y2006C67）.
