Zheng Guo, Xinxin Lv, Jianwen Li, Shiping Yue, Jing Du
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引用次数: 0
Abstract
Background
Cell polarization is an important morphological process that is crucial for the formation and function of tissues and organs. The blastocyst cavity expansion is an apparent event during the second cell fate specification in mouse embryos, yet its impact on cell polarization remains unclear. In this study, we investigate the effects of blastocyst cavity expansion on cell polarization.
Methods
The methods of this study involve hyperosmotic treatment or disruption of TE cortical tension by laser ablation, combined with immunofluorescence.
Results
We found that inhibition of the blastocyst cavity expansion through hypertonic treatment or disruption of TE cortical tension by laser ablation suppresses the levels of the ζ isotype of protein kinase C (PKC ζ) which is a member of the atypical PKC subfamily involved in cell polarization. We further found that during the embryonic stages E3.5 to E4.0, the expression of extracellular signal-regulated kinase 1 (ERK1), a key upstream regulator of PKC ζ, is altered in a similar tendency to that of PKC ζ, indicating a potential regulatory function of ERK1 in cell polarization during early development of mouse embryos.
Conclusions
This study reveals the function of the mechanical behavior of embryos in cell polarization of early mammalian embryos. The relationship between cell polarization and blastocyst cavity expansion in early embryonic development provides a new understanding, thereby offering fresh insights for the screening and detection of indicators for normal blastocyst development.
期刊介绍:
The journal Birth Defects Research publishes original research and reviews in areas related to the etiology of adverse developmental and reproductive outcome. In particular the journal is devoted to the publication of original scientific research that contributes to the understanding of the biology of embryonic development and the prenatal causative factors and mechanisms leading to adverse pregnancy outcomes, namely structural and functional birth defects, pregnancy loss, postnatal functional defects in the human population, and to the identification of prenatal factors and biological mechanisms that reduce these risks.
Adverse reproductive and developmental outcomes may have genetic, environmental, nutritional or epigenetic causes. Accordingly, the journal Birth Defects Research takes an integrated, multidisciplinary approach in its organization and publication strategy. The journal Birth Defects Research contains separate sections for clinical and molecular teratology, developmental and reproductive toxicology, and reviews in developmental biology to acknowledge and accommodate the integrative nature of research in this field. Each section has a dedicated editor who is a leader in his/her field and who has full editorial authority in his/her area.