ABSTRACT
In recent years,microRNAs(miRNAs)have been detected at different stages of follicular development and in different cells of follicles.Extracellular vesicle(EV)-derived miRNAs have also been detected in the follicular fluid of mature follicles.miRNAs participate in the regulation of normal follicular development,and the regulation disorder may lead to the occurrence of some ovarian diseases.In order to further systematically elucidate the regulatory mechanism of miRNAs on follicular development and find suitable EV-derived miRNAs that can predict oocyte development,we reviewed the functions of miRNAs in follicular development from the perspectives of granulosa cell development,oocyte development,and hormone synthesis.
Subject(s)
Female , Humans , Follicular Fluid , Granulosa Cells , MicroRNAs/genetics , Oogenesis , Ovarian FollicleABSTRACT
<p><b>OBJECTIVE</b>To determine the regulatory role and mechanism of nitric oxide (NO) in the development and hatching of mouse blastocysts.</p><p><b>METHODS</b>The Kunming female mice were superovulated and then mated with mature male mice. On the day 2.5 of their pregnancy, morulae were flushed from their uterine horns with culture media. Morulae were cultured in different concentrations of N-nitro-L arginine methyl ester (L-NAME), sodium nitroprusside (SNP), or the combination of L-NAME and SNP in culture media for 48 hours. The development and hatching of blastocysts were examined on day 4 and day 5 and the total numbers of blastocyst cells and cysteinyl aspartate specific proteinase 3 (caspase 3) were observed under confocal laser scanning microscope.</p><p><b>RESULTS</b>With the increase of the concentration of L-NAME or SNP, the hatching rate of blastocysts and the total number of blastocyst cells were significantly reduced. The addition of 10 nmol/L SNP in culture media with 5 mmol/L L-NAME significantly increased the development of blastocysts and promoted hatching of blastocysts. However, with increase of SNP concentration in culture media with 5 mmol/L L-NAME, the development and hatching rates of blastocysts were significantly decreased. L-NAME had no obvious effect on the expression of active caspase 3 in blastocyst cells. However,when being above 500 nmol/L,SNP significantly increased the expression of caspase 3 in blastocyst cells.</p><p><b>CONCLUSIONS</b>NO plays an important role in development and hatching of mouse blastocysts. Excessively high or low NO can damage the division of blastomeres, resulting in the failure of the blastocyst development and hatching. Also, excessively high NO can lead to the apoptosis of the blastocyst cells.</p>
Subject(s)
Animals , Female , Humans , Male , Mice , Pregnancy , Arginine , Blastocyst , Culture Media , Nitric Oxide , Nitroprusside , UterusABSTRACT
Many pathological phenomena of male infertility are related to epigenetic changes in male germ cells. Epigenetic regulation during spermatogenesis plays an important role in mitotic/meiotic divisions and spermiogenesis. The histones have various post-translational modifications on different amino acid residues during spermatogenesis. These modifications are crucial to the precise regulation of spermatogenesis. Moreover, the histone-to-protamine transition will occur during spermiogenesis. Many studies have also found that abnormal changes of histone modifications during spermatogenesis may damage the sperm development, leading to male sterility. This article reviews the changes of histone modifications during spermatogenesis, the regulation of the development of male germ cells, and the relationship between histone abnormalities and male sterility.
Subject(s)
Humans , Male , Epigenesis, Genetic , Histones , Metabolism , Infertility, Male , SpermatogenesisABSTRACT
<p><b>OBJECTIVE</b>To determine the effects of bisphenol-A (BPA) on blastocyst development and implantation.</p><p><b>METHODS</b>According to completely randomized grouping method, 90 pregnant mice were divided into 100, 300, and 600 mg/(kg·d)BPA groups and control group. BPA-treated pregnant mice were orally administered with BPA at concentrations of 100, 300 and 600 mg/(kg·d) from day 0.5 to day 3.5 of their pregnancy. Blastocyst implantation and development were studied.</p><p><b>RESULTS</b>In the 300 mg/(kg·d) BPA group, the number of implantation sites and implantation rate were significantly decreased. In the 600 mg/(kg·d) group, no implantation sites were observed among pregnant mice and BPA inhibited embryo implantation. Blastocyst development on day 4 was examined, and findings showed that the development rate and total numbers of blastocysts in BPA treatment groups had no significant difference from the control group. However, BPA at 300 and 600 mg/(kg·d) significantly reduced blastocyst hatching rate and dramatically increased the number of blastocyst apoptotic cells when compared with those in the control group.</p><p><b>CONCLUSION</b>BPA at a high concentration damages the blastocyst development before implantation and inhibits embryo implantation.</p>
Subject(s)
Animals , Female , Male , Mice , Pregnancy , Benzhydryl Compounds , Pharmacology , Blastocyst , Embryo Implantation , Phenols , PharmacologyABSTRACT
Bisphenol A (BPA) is a commonly used phenolic environmental estrogen. Long-term exposure of female mammalians to BPA can lead to endocrine disorders, followed by the morphological and functional changes in ovary, uterus, vagina, and oviducts. The interactions of BPA with various target molecules or tissues will cause different effects. To further elucidate the effects of BPA on female reproductive system, we review the changes in the structure and functions of female reproduction system after BPA exposure and their possible mechanisms.