Mullerian inhibiting substance induces apoptosis of human endometrial stromal cells in endometriosis.

Context: Müllerian inhibiting substance (MIS) is produced in Sertoli cells of fetal testis and causes regression of müllerian ducts in male embryos. MIS also can induce the cell cycle arrest and apoptosis in müllerian duct-derived tumors in vivo and in vitro.

Objective: Our objective was to investigate the expression of MIS type II receptor (MISR II) and whether MIS can inhibit the proliferation and induce apoptosis in primary cultures of endometrial stromal cells (ESC) of endometriosis.

Expression of Müllerian inhibiting substance type II receptor and antiproliferative effects of MIS on human cervical cancer.

This study aimed to analyze expression of Müllerian inhibiting substance type II receptor (MISRII) protein and mRNA in cervical neoplasia, to demonstrate the growth inhibition of cervical cancer cells by administration of highly purified recombinant human Müllerian inhibiting substance (MIS) and, furthermore, to evaluate the clinical significance of MIS as a biological modifier for MIS receptor expressing tumors. Reverse transcriptase polymerase chain reaction (RT-PCR) was used for MISRII mRNA expression, and in situ hybridization and immunohistochemistry were used to observe expression, location of MISRII mRNA and protein, respectively. To demonstrate the effect of MIS on the viability of cervical cancer cells, methyl thiazole tetrazolium (MTT) assay was performed.

Antioxidant effects of equol on bovine aortic endothelial cells.

This study is to examine the effects of equol on the H(2)O(2)-induced death of bovine aortic endothelial cells (bAECs) and the mechanism of its protective effects. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide] assay showed that in the control group, cell survival rate decreased significantly, each in proportion to the duration of the H(2)O(2) stimulation (P<0.05), but, in the equol-pretreated group, such decrease was not statistically significant.