ABSTRACT
OBJECTIVE: The aim of this study was to detect the effects of varying tissue sizes on the efficiency of baboon ovarian tissue vitrification. STUDY DESIGN: The percentages of morphologically normal primordial follicles and the follicles expressing bax protein in ovarian tissues after vitrification-warming were measured. Besides, the 17-ß estradiol levels in the culture supernatants were measured. RESULTS: The percentages of morphologically normal primordial follicles in vitrified-warmed ovarian tissues slicing in 0.5-1.5mm in length and wide, and 1.0mm in thickness were significantly higher than those slicing in 2.0mm in length and wide, and 1.0mm in thickness. Moreover, the follicles expressing bax protein in vitrified-warmed ovarian tissues slicing in 0.5-1.5mm in length and wide, and 1.0mm in thickness were significantly lower than those slicing in 2.0mm in length and wide, and 1.0mm in thickness. The 17-ß estradiol levels in the culture supernatants slicing in 1.0-1.5mm in length and wide, and 1.0mm in thickness were significantly higher than those slicing in 0.5mm or 2.0mm in length and wide, and 1.0mm in thickness. CONCLUSIONS: Cortex piece slicing in 1.0-1.5mm in length and wide, and 1.0mm in thickness is suitable for baboon ovarian vitrification.
Subject(s)
Cryopreservation/methods , Estradiol/metabolism , Ovarian Follicle/metabolism , bcl-2-Associated X Protein/biosynthesis , Animals , Cells, Cultured , Female , Organ Size/physiology , Ovarian Follicle/physiology , Papio , VitrificationABSTRACT
PURPOSE: To evaluate the long-term effects of superovulation on fertility and sexual behavior of male offspring in mice. METHOD: The mice were superovaluted, and the fertility of male offspring (F1 generation and F2 generation) were evaluated in terms of the percentage of plugs and pregnancies, serum testosterone concentrations, and sperm motility. Furthermore, the sexual behavior of male offspring and sex ratio (F1 generation and F2 generation) were measured. RESULTS: There were no significant differences in the percentage of plug and pregnancies, serum testosterone concentrations, sperm motilities and sex ratio between the offspring in naturally conceived group and superovulation groups (both F1 generation and F2 generation). The sperm hyperactivity at 90 min after incubation of F1 generation in naturally conceived group were higher than that of F1 generation in superovulation group, but the differences did not reach statistical significance. The offspring produced by superovaluted oocytes (both F1 generation and F2 generation) did not exhibit significant alterations in sexual behavior. CONCLUSIONS: No significant alterations were found in fertility and sexual behavior of male offspring in mice produced by superovaluted oocytes compared with those of naturally conceived offspring.
Subject(s)
Fertility/physiology , Sexual Behavior, Animal/physiology , Superovulation/physiology , Animals , Female , Male , Mice, Inbred C57BL , Oocytes/physiology , Ovulation Induction , Pregnancy , Sex Ratio , Sperm Count , Sperm Motility , Testosterone/bloodABSTRACT
Programmed cell death 4 (PDCD4) is a newly identified tumor suppressor that can inhibit activator protein (AP)-1 activation and protein translation. Our previous studies indicate that lost or reduced PDCD4 expression is associated with the progression of ovarian carcinoma. However, direct evidence that PDCD4 inhibits malignant phenotype of human cancer cells is limited. In the present study, we found that PDCD4 expression in ovarian cancer cell lines (SKOV3, 3AO, and CAOV3) inhibited significantly their proliferation and cell cycle progression, and induced apoptosis. More importantly, up-regulation of PDCD4 expression decreased the colony-forming capacity of ovarian cancer cells in vitro and tumorigenic capacity in mice. These results demonstrate that PDCD4 can suppress the malignant phenotype of ovarian cancer cells, and may represent a novel therapeutic target for the treatment of ovarian cancer.
Subject(s)
Apoptosis Regulatory Proteins/metabolism , Carcinoma/pathology , Ovarian Neoplasms/pathology , RNA-Binding Proteins/metabolism , Animals , Apoptosis/genetics , Apoptosis Regulatory Proteins/genetics , Apoptosis Regulatory Proteins/physiology , Carcinoma/genetics , Cell Cycle , Cell Line, Tumor , Cell Proliferation , Female , Gene Expression Regulation, Neoplastic , Genes, Tumor Suppressor , Humans , Immunohistochemistry , Mice , Mice, Nude , Ovarian Neoplasms/genetics , RNA-Binding Proteins/genetics , RNA-Binding Proteins/physiology , Random Allocation , Transcription Factor AP-1/antagonists & inhibitors , Transfection , Tumor Burden , Xenograft Model Antitumor AssaysABSTRACT
OBJECTIVE: To study the inhibitory effect of endostatin mediated by lipofectin on transplanted ovarian cancer in nude mice. METHODS: Constructed recombinant vector pVAX1-sEn expressing human endostatin protein was transfected into ovarian cancer cell line 3AO by lipofectin. mRNA of endostatin was detected by RT-PCR. The expression of endostatin in supernatants was detected by enzyme-linked immunosorbent assay (ELISA). The inhibitory effect of pVAX1-sEn on endothelial cell line ECV-204 was detected by methyl thiazolyl tetrazolium (MTT). By use of lipofectin mediated pVAX1-sEn for intratumor injection, the inhibitory effect on growth of ovarian cancer was observed. RESULTS: The result of RT-PCR showed there was a specific band at 610 bp. The expression quantity of endostatin in transfected cell supernatant was (201 +/- 8) ng/ml by ELISA. MTT showed pVAX1-sEn transfected cell supernatant could effectively inhibit the growth of ECV-204, the highest inhibitory ratio was 42%. The tumor volumes in pVAX1-sEn treatment group was (0.85 +/- 0.18) cm(3), significantly smaller than that in normal saline control group (1.90 +/- 0.28) cm(3) and pVAX1 control group (1.78 +/- 0.32) cm(3) (P < 0.05). HE stain in tumor tissue showed that there were obvious necrosis cells in the pVAX1-sEn treatment group, but there were flourishly growing tumor cells in pVAX1 and normal saline control groups. CONCLUSION: pVAX1-sEn mediated by lipofectin can effectively inhibit the growth of ovarian cancer.