SJ-10 Recoverable Satellite for Space Microgravity Experiments

SJ-10 is a recoverable scientific experiment satellite specially for the space experiments of microgravity physics science and space life science.This mission was officially started on 31 December 2012,and the satellite was launched on 6 April 2016.This paper introduces briefly the SJ-10 mission,the progress of SJ-10 engineering and the project constitution of sciences experiments onboard SJ-10.The purpose of this mission is to discover the law of matter movement and the rule of life activity that cannot be discovered on the ground due to the existence of gravity,and to know the acting mechanism on organisms by the complex radiation of space that cannot be simulated on the ground.

太空环境下哺乳动物胚胎发育和生殖研究进展及展望

随着人类太空探索进程的加速和深入,哺乳动物能否在太空完成生命孕育和后代繁衍成为科学界及公众关注的问题.过往研究提示,太空飞行会对哺乳动物胚胎发育和生殖功能造成某些潜在的危害,这些危害的产生与太空存在的特殊环境有关,如宇宙辐射和重力等变化.本文首先综述了国内外利用空间飞行器搭载平台、地基微重力和辐射平台开展哺乳动物生殖和发育研究的进展,还特别论述了本团队利用实践十号(SJ-10)返回式科学卫星开展的太空条件下哺乳动物早期胚胎体外发育研究结果,随后展望了未来借助科学实验卫星、空间站、月球和火星探测等太空飞行实验平台进行动物生殖功能和胚胎发育研究的着重点.未来要实现哺乳动物乃至人类在地外空间的生存繁衍,阐明微重力、宇宙辐射或其他空间环境因素对哺乳动物胚胎发育和生殖生理的影响是至关重要的,在此基础上方可采取各种有针对性的保护措施,成功实现地外生命繁衍.

Induction of matrix metalloproteinase-9 and-2 activity in mouse blastocyst by fibronectin-integrin interaction

Fibronectin, a major extracellular matrix, plays an important role in embryo implantation by mediating embryo adhesion and outgrowth. In this work, mouse blastocysts produced pro-matrix metalloproteinase-9, pro-matrix metalloproteinase-2 and 64 ku matrix metalloproteinase-2 when they were co-cultured with fibronectin. In contrast, mouse blastocysts did not produce these proteinases without fibronectin. Focal adhesion kinase is a fundamental molecule of integrin signaling pathway and its antisense oligodeoxynucleiotide inhibited blastocyst matrix metalloproteinases expression induced by fibronectin. The results indicated that fibronectin triggered matrix metalloproteinase-9 and -2 expression in mouse blastocyst through its integrin receptors and subsequent signaling pathway, which enhanced the synchronization of blastocyst invasiveness and uterine receptivity and ensured the accuracy of events relative to implantation in timing and spatiality.

Expression, distribution and function of the focal adhesion kinase (pp125^(FAK)) during murine ectoplacental cone outgrowth in vitro

Mouse embryo implantation is a complex process that includes trophoblast cells derived from ectoplacental cone (EPC) adhesion to and migration through the extracellular matrix (ECM) of uterine endometrium and invasion into the decidua. At the time of implantation, fibronectin (FN) is abundant in the decidua and is distributed pericellularly around each individual stromal cell, and its receptor (integrin α-5β-1) expression on trophoblast populations is up-regulated. The focal adhesion kinase, a 125 ku protein tyrosine kinase (pp125 FAK), is tyrosine phosphorylated upon integrin engagement with its ECM ligand, and its tyrosine phosphorylation sites then serve as the binding sites which couple it with cellular proteins that contain Src SH2 or SH3 domains. Through these linkages, pp125 FAK may integrate multiple signals triggered by integrins. The model of EPC culture %in vitro% was used to study the expression, distribution and function of pp125 FAK during EPC outgrowth on FN. Results indicated that, pp125 FAK primarily expressed and distributed in cellular focal adhesions of the front edge of trophoblast outgrowth from EPC, and was localized in the peripheral region of the individual migrating trophblast cell; antibody or antisense oligodeoxynucleotide to pp125 FAK inhibited EPC attachment and outgrowth, as well as trophoblast cells spreading and migration. This experiment demonstrated that pp125 FAK as an integrin-mediated signaling molecule was involved in EPC outgrowth %in vitro%, and played an important role during trophoblast cells interaction with FN.

Effects of vascular endothelial growth factor on MMPs during embryo implantation in mice

Vascular endothelial growth factor (VEGF) is a specific mitogen of endothelial cells and plays an important role in vasculogenesis and angiogenesis. In recent years, both our and other laboratories have found that VEGF may be involved in embryo implantation. However, the relationship between VEGF and MMP-2 and MMP-9, the marker molecules of embryo implantation, is still unknown. In the present study, an examination of the effects of VEGF on the expression and secretion of MMP-2 and MMP-9 during implantation in mice was carried out by RT-PCR and gelatin zymography. The results show that VEGF antibody significantly decreased uterine mRNA levels of MMP-2 and MMP-9 during pregnancy, and that VEGF could up-regulate the activities of MMP-2 and MMP-9 secreted by blastocysts cultured in vitro in a time- and dose-dependent manner. The results suggest that, in the course of implantation, the ability for metastasis and invasion of blastocysts and the receptive-ness of the uterus might be regulated by VEGF

Embryo implantation:A time for recalling and forwarding

The success of embryo implantation is a critical step towards further embryo development and pregnancy outcome. The observations and investigations on embryo implantation have been over a century. A huge body of knowledge has been accumulated in anatomy, histology, ultrastructure and hormonal regulation; as well as recently in depth information about molecular signaling pathways got from studies of genomic wide gene screening and specific gene deletion. The knowledge from basic research has also substantially helped to initiate and improve the Artificial Reproductive Technology (ART) in clinical applications. Now we've known that the normal embryo implantation involves the embryo's development into an implantation-competent blastocyst and the synchronized transformation of uteri into a receptive stage. The interdependent relationship between the blastocyst and uterus involves complicated hormonal regulation and local paracrine, juxtacrine interactions. In this paper, we review some important historical findings regarding uterine receptivity and blastocyst activation, as well as some less discussed topics such as embryo spacing, embryo orientation. Further understandings on detailed mechanisms during the process of embryo implantation will help cure women infertility as well as develop new generation of non-steroids contraceptives.

Determinants of uterine aging:lessons from rodent models

The uterus is an indispensable organ for the development of a new life in eutherian mammals.The female mammalian reproductive capacity diminishes with age.In this respect,the senescence of uterine endometrium is convinced to contribute to this failure.This review focuses on the physiological function of the uterus and the related influence of aging mainly in rodent models.A better understanding of the underlying mechanisms governing the process of uterine aging is hoped to generate new strategies to prolong the reproductive lifespan in humans.

Effect of matrix metalloproteinase-26(MMP-26) during embryo implantation in the mouse

Matrix metalloproteinase-26 (MMP-26, endo-metase and matrilysin-2), a novel member of the MMPs family, is detected not only in the placenta and uterus, but is widely expressed in malignant tumors from different sources as well as in diverse tumor cell lines. However, the function of MMP-26 in the reproductive system has never been reported. Expression of MMP-26 in mouse embryos and the function of the MMP-26 antibody during mouse embryo implantation was examined for the first time by injecting the uterine horn, immunohistochemistry, in situ hybridization, co-culture of mouse blastocysts and uterine monolayer epithelial cells, Western blot, RT-PCR, Northern blot and zymography. Our results show that there is strong expression of MMP-26 niRNA and protein in the mouse embryo. Furthermore, the MMP-26 antibody dramatically inhibited mouse embryo implantation and significantly inhibited adhesion and outgrowth of mouse blastocysts on in vitro uterine monolayer epithelial cells. At the same time, the MMP-26

Advances in the study on induced pluripotent stem cells

Recently, the study on "induced pluripotent stem cells" (iPS cells) has made a great breakthrough, and it is considered as a new milestone in the history of life science. This progress has updated our tradi-tional concepts about pluripotency control, and provided people with a brand-new strategy for somatic cell nuclear reprogramming. In virtue of its availability and stability, this method holds great potential in both biological and clinical research. In order to introduce this rising field of study, this paper starts with an overview of the development of iPS cell establishment, describes the key steps in generating iPS cells, elaborates several relevant scientific issues, and evaluates its current restrictions and promises in future research.

Regulation of mouse blastocyst adhesion,outgrowth and matrix metalloproteinase-2 by focal adhesion kinase

The interaction of extracellular matrix-integrin markedly influences the adhesion, outgrowth, differentiation and expression of serine proteinases by the blastocyst, so it is regarded as a vital factor in blastocyst implantation. Al- though the mechanism of extracellular interactions between extracellular matrix and integrins has been well elucidated, the roles of the signaling molecules in the extracellular ma- trix-integrin signal transduction pathway in blastocyst im- plantation are unknown. This limits the understanding of blastocyst implantation and ECM-integrin signal transduc- tion pathway. In the present study, in vitro blastocyst culture and indirect immunocytochemistry, matrix metallopro- teinases (MMPs) zymography and antisense oligodeoxynu- cleotide (ODN) were used to investigate the expression of a fundamental molecule of integrin-dependent signal trans- duction pathways, focal adhesion kinase (FAK), in mouse blastocysts and its influence on mouse blastocyst adhesion, outgrowth and MMP-2. The results showed that mouse blas- tocysts expressed FAK. FAK protein was clustered in the peripheral migrating trophoblast cells and dispersed in the central area of blastocyst outgrowth. Fibronectin triggered pro-MMP-2 and 64 kD MMP-2 activities. The antisense ODN to FAK attenuated pro-MMP-2 and 64 kD MMP-2 activities which decreased abruptly and tended to disappear with increasing concentrations of the antisense ODN. Both mouse blastocyst adhesion and outgrowth on fibronectin were also influenced by the antisense ODN. Up to 20 mg/mL of the antisense ODN concentration, the adhesion and out- growth rates were decreased in a dose-dependent manner. The results indicated that FAK influenced mouse blastocyst adhesion, outgrowth and MMP-2 activity by intracellular signal transduction. In other words, FAK regulates mouse implantation in terms of blastocyst adhesive and invasive abilities.