Response of porcine epithelial rests of Malassez to stimulation by interleukin-6.

AIM: To investigate the proliferation and migration of epithelial cell rests of Malassez (ERM) after stimulation with IL-6. METHODOLOGY: Porcine-derived ERM were seeded on Dulbecco's modified Eagle's Medium, and IL-6 (100 pg mL-1 ) was incorporated into the culture medium. The WST-1 assay was performed to evaluate cell proliferation, and absorption was measured at 450 nm. A wound-healing assay and immunofluorescence assay for integrin α3 were conducted to investigate migration. The Kruskal-Wallis test and the Mann-Whitney U-test with Bonferroni correction were used to analyse data of WST-1 and wound-healing assays. RESULTS: Cell proliferation following the stimulation by IL-6 increased over time, with a significant increase being observed at 6 h (P < 0.05), but not in a concentration-dependent manner. Cell proliferation was significantly greater in IL-6-treated ERM than in nontreated ERM (P < 0.05). The results of the wound-healing assay revealed earlier closure in IL-6-treated ERM (P < 0.05). In the immunofluorescence assay, integrin α3 was detected at the edge of cell processes adjacent to the wound area. A neutralized antibody abrogated the effects of the IL-6 stimulation in cell proliferation and migration. CONCLUSION: IL-6 promoted the proliferation and migration of porcine ERM in vitro.

Actin stabilization induces apoptosis in cultured porcine epithelial cell rests of Malassez.

AIM: To test whether actin stabilization by jasplakinolide induces inhibition of cell viability and apoptosis in epithelial cell rests of Malassez (ERM). METHODOLOGY: ERM derived from porcine were spread in a 96-well dish (5 × 10(4) /well) using Dulbecco's modified Eagle's medium. The actin-specific stabilization reagent, jasplakinolide, was incorporated into the culture medium and incubated for 24 h. To evaluate cell viability, the WST-1 assay was carried out and absorption (450 nm) was measured. To detect apoptotic cells, monoclonal antibody to single-strand DNA (ssDNA) was used and absorption (405 nm) was measured. Actin stabilization and apoptosis induced by jasplakinolide were morphologically investigated by staining with Alexa Fluor 568 phalloidin and observed under a fluorescent microscope. As a negative control, DMSO was used instead of jasplakinolide. Differences between the jasplakinolide-treated group and the control group were analysed statistically using the Student's t-test. RESULTS: Cell viability decreased in a concentration-dependent manner, and cell viability in the jasplakinolide-treated ERM was lower than that in nontreated ERM (n = 16, P < 0.01). Apoptotic cells in the jasplakinolide-treated ERM were more frequently detected compared to that in nontreated ERM (n = 16, P < 0.01). Morphologically, shrinkage, irregular forms and fragmentation of nuclei suggesting apoptotic bodies were observed in jasplakinolide-treated ERM, whilst actin filaments were extended in non-treated ERM. CONCLUSION: Actin stabilization by jasplakinolide inhibited cell viability and induced apoptosis in epithelial cell rests of Malassez.

Effects of captopril on the hypertrophied heart of essential hypertensive patients.

Changes in blood pressure and heart rate after exercise, left ventricular wall thickness, ejection fraction and left ventricular mass were examined by echocardiography before and at the 8th week administration of captopril (37.5-75.0 mg/day) in 11 patients with essential hypertension. The blood pressure showed a gradual and significant decrease from the second week of captopril administration, but the heart rate remained unchanged. No changes were observed in the blood pressure or heart rate after exercise, nor before, during and after the administration of captopril. In the echocardiographic examinations, the wall thickness decreased significantly from 12.1 +/- 2.1 mm before administration to 10.6 +/- 1.5 mm at the 8th week of administration in the interventricular septum, from 11.2 +/- 1.8 mm to 10.1 +/- 1.5 mm in the left ventricular posterior wall, and the left ventricular mass in parallel decreased from 266 g to 218 g. In 7 patients, whose wall thickness was 12 mm or more, the thickness of the septum decreased significantly from 13.9 +/- 1.2 mm to 11.7 +/- 2.1 mm and that of the left ventricular posterior wall from 12.6 +/- 1.5 mm to 10.6 +/- 1.8 mm. Captopril administration produced regression of cardiac hypertrophy in patients with essential hypertension within a period of only 8 weeks.